Scottish Doctor, author, speaker, sceptic

What happens to the carbs?

I have found a strange thing happens when I talk to nutritionists about the fate of carbohydrates in the human body. Professors, who shall be nameless, appear unable to admit how basic human physiology works. For example, they may concede a few steps here and there, but they will never, ever, admit to the following chain that I have described below.

1: Carbohydrates, such as fruit and vegetables, bread, pasta… and, of course, less complex sugars – such as the stuff we sprinkle on cornflakes, that we call ‘sugar’, are all turned into simple sugars in the human digestive tract before entering the bloodstream.

2: If you keep eating carbohydrate the resultant simple sugars will, at first, be stored. The human body can pack away around 1,500 calories of sugar. However, once this limit is reached, the liver will turn the rest into fat.

3: The fat that is made in the liver is palmitic acid

4: The next step is that three palmitic acid molecules are attached to a glycerol molecule, to form a triglyceride.

5: These triglycerides will then be packed into Very Low Density Lipoproteins (VLDL) and released into the bloodstream. [Beware of confusion here. For VLDLs are also called triglycerides although, of course, they are not. VLDLs contain triglycerides but they are not the same thing – even if they are called the same thing].

6: When VLDLs reach fat cells (adipose tissue), the triglyceride is stripped out and absorbed into fat cells. Which means that VLDLs gradually shrink.

7: Once a VLDL has lost a large amount of triglyceride it becomes a new, smaller, lipoprotein, which is often referred to as ‘bad cholesterol’ a.k.a. LDL (Low Density Lipoprotein).

8: LDL is taken out of the circulation, primarily, by the liver. Some LDLs are removed from the circulation by other cells around the body that need the cholesterol contained in them.

9: As can be seen, the only source of LDL is VLDL.

Here a couple of quotes from Wikipedia to confirm at least a couple of these steps:

Lipogenesis is the process by which acetyl-CoA is converted to fatty acids. The former is an intermediate stage in metabolism of simple sugars, such as glucose, a source of energy of living organisms. Through lipogenesis and subsequent triglyceride synthesis, the energy can be efficiently stored in the form of fats.

Lipogenesis encompasses both the process of fatty acid synthesis and triglyceride synthesis (where fatty acids are esterified with glycerol to form fats). The products are secreted from the liver in the form of very-low-density lipoproteins (VLDL). VLDL are secreted directly into blood, where they mature and function to deliver the endogenously derived lipids to peripheral tissues.https://en.wikipedia.org/wiki/Lipogenesis

Excess carbohydrates in the body are converted to palmitic acid. Palmitic acid is the first fatty acid produced during fatty acid synthesis and the precursor to longer fatty acids. As a consequence, palmitic acid is a major body component of animals. In humans, one analysis found it to comprise 21–30% (molar) of human depot fat and it is a major, but highly variable, lipid component of human breast milk.https://en.wikipedia.org/wiki/Palmitic_acid

I am half tempted to leave the blog here and let you think about what all of that means for a while. However, I feel the need to make a couple of other points, in no particular order. First, I would like you to think about this fact. The form of fatty acid that the liver chooses to synthesize from sugar(s) is palmitic acid, a saturated fat. Palmitic acid is also the major component of breast milk.

Yet, despite this, we are told that saturated fats are uniquely unhealthy, and eating them leads to heart disease. Indeed, within to the very same Wikipedia article on palmitic acid we learn that: ‘According to the World Health Organization, evidence is “convincing” that consumption of palmitic acid increases risk of developing cardiovascular diseases.’

It seems that we are being asked to believe that the body naturally synthesizes a substance, palmitic acid, that actively damages our health. Not only that, but mothers choose to synthesize exactly the same form of fatty acid in their breast milk, which then increase the chances of their offspring developing cardiovascular disease.

Now just how likely does this seem…exactly? We have evolved to kill ourselves from heart disease? As Spock may have said, ‘its evolution Jim, but not as we know it.’ You would think that if polyunsaturated fats were healthy, this is what the human body might choose to make. But no, we eat super healthy fruit and vegetables and then our body, in a unique and ironic twist of fate, converts them into death dealing saturated fatty acids.

Not only that, but just to rub salt into the wounds, once the liver has synthesized these death dealing fatty acid molecules it then chooses to pack them into VLDLs which have the cheek to shrink down into LDL a.k.a. ‘cholesterol’ and these also kill us with heart disease (allegedly).

Of course, if you actually eat saturated fat, this gets nowhere near the liver. It is digested, packed into chylomicrons, and these very large lipoproteins enter the bloodstream directly through the thoracic duct. Which is a secret passage from the gut that opens out in one of the veins in your neck. When chylomicrons encounter fat cells, the fats/triglycerides are sucked out, and the chylomicron shrinks down to virtually nothing. Chylomicrons, however, do not convert to LDL and have nothing whatsoever to do with heart disease – even according to those who think saturated fat in the diet is deadly.

Yet, despite this knowledge we are continuously told, in all seriousness, that eating saturated fat raises our LDL levels and causes us to die prematurely of heart disease. [You may have noticed that cholesterol has hardly entered this discussion at any point.] When people ask me why I don’t believe in the diet/heart hypothesis, I tend to shrug and move the conversation on.

However, if I am feeling a bit stroppy I tend to reply that ‘Even if you were to believe that a raised LDL levels causes heart disease, the current diet/heart hypothesis does not, and cannot make any sense from a biological or physiological perspective.’ If you were actually looking for a substance that really could raise LDL/cholesterol levels it would have to be carbohydrates a.k.a. sugars. After all the only source of LDL is VLDL, and it is eating too much sugar that raises VLDL levels.

In short, how can it not be that carbohydrates raise LDL levels? This is what a basic understanding of lipid physiology tells us must be true. Yet, people write papers on this phenomenon in a tone of almost stunned surprise. Here for example is a paper called ‘The Effect of Dietary Carbohydrate on Triglyceride Metabolism in Humans’:

When the content of dietary carbohydrate is elevated above the level typically consumed (>55% of energy), blood concentrations of triglycerides rise. This phenomenon, known as carbohydrate-induced hypertriglyceridemia, is paradoxical because the increase in dietary carbohydrate usually comes at the expense of dietary fat. Thus, when the content of the carbohydrate in the diet is increased, fat in the diet is reduced, but the content of fat (triglycerides) in the blood rises. http://jn.nutrition.org/content/131/10/2772S.full#fn-1

This author, writing for the Journal of Nutrition, finds it paradoxical that… increased dietary carbohydrate usually comes at the expense of dietary fat….but the content of fat (triglycerides) in the blood rises. Well, what did they think would happen? That carbohydrates would turn into fairies at the bottom of the garden?

Once the liver and muscles are full of sugar (stored as glycogen – a polymer of glucose) the body can do absolutely nothing else with it, but turn it into fat – through the processes I have described earlier. This is basic, incontrovertible science.

Most people who are interested in the potential benefits of the low carb high fat diet (LCHF), have tended to look at it from the perspective of helping with controlling diabetes, and promoting weight loss. I came at the LCHF diet from my own perspective, which is heart disease.

When you understand the science you find yourself looking at the diet heart hypothesis (fat in the diet raises LDL levels, which causes heart disease) and thinking. This does not make any sense at all. Yet, such is the determination of the nutritional experts to defend their position that they never, ever, talk about ‘what happens to the carbs?’

What happens to the carbs is that they are all turned into saturated fat. This then raises VLDL levels and these, in turn becomes LDL. Yet eating carbs is supposed to be healthy, and eating saturated fat is unhealthy. Go figure.

Dr. Malcolm Kendrick posted: “I have found a strange thing happens when I talk to nutritionists about the fate of carbohydrates in the human body. Professors, who shall be nameless, appear unable to admit how basic human physiology works. For example, they may concede a few steps here”

I knew that much. Just wondered about the mechanism (my original question was obviously badly worded). I am genuinely interested.

Incidentally, your book (recommended by my GP) was the start of my own research into health and one of a number of things I read that enabled me to ignore the advice I was given and come off / refuse medication (including statins) and end up improving all bio-markers of metabolic syndrome (including cholesterol, which is now “perfect” according to the believers).

Again, correlation does not equal causation, but darn if a lot of evidences doesn’t point to insulin resistance being bad. (Including low HDL, which is also associated with insulin resistance; improve your insulin resistance and HDL goes up. Now, HDL is likely a marker for something, but that something might be insulin resistance.)

Bob M. you’ve got it absolutely right. I’ve been a follower of Dr. Atkins and Dr. Michael Eades for a long, long time, and it is good to see more explanation of the “how” Triglycerides are made. That was a missing link for me.

Also, Lipoprotein Lipase (LPL) is more likely to uptake fatty acids into fat cells in the presence of insulin – at least at the micro level…I’m not sure if there’s widespread agreement about whether this is happening at a more macro level or not, and clearly the effects of insulin are amplified in folks whose cells are (or have become) resistant to insulin

Bravo! You’re such great fun to read. Methinks we’ll have to wait for all the idiots to die off before anything changes. On this side of the pond the USDuh rearranges the deck chairs on the Titanic every five years, and this year, surprise, surprise, they’ve exonerated dietary cholesterol (but keep shoving sugar and bread into your belly, and stay away from saturated fat, children).

I have never found any good explanation of how satfat raises LDL levels.
Last time I researched the only thing I found was something about downregulating LDL receptors.
Stephan Guyenet did not find anything either in this articlehttp://wholehealthsource.blogspot.no/2011/01/does-dietary-saturated-fat-increase.html

Well, what did they think would happen? That carbohydrates would turn into fairies at the bottom of the garden?

LOL! I think you’re on to something there. How else would we get fairies at the bottom of the garden? Photosynthesis?

Some 40 years ago, I acquired an A level in Biology. I remember learning how the various macronutrients were broken down and digested. There were no fairies involved. Nor were any carbohydrates treated differently from others — there were no “good” carbs or “bad” carbs. The only thing that differed between them was how long they took to get digested.

Absolutely bloody marvelous!
Agree with every word, especially after my whisky and ginger tonight!
Seriously though, surely other medics know this? If not, why not?
By the way, although I have been low-carbing for over 2 years, and seeing marvelous results, I am now looking at the concept of reintroducing bread into my diet, albeit in smaller quantities than when instructed to consume 55% CHO according to the NHS diabetic lifestyle dictat.
Only now I am being very fussy regarding the source of my grains/flour, and I am closely following Andrew Whitley regarding his pronouncements on sourdough techniques.

Thanks David. I was sourcing flour on the net last night and came across the Einkorn by Doves Farm
I have never actually tried their Einkorn. Maybe Waitrose do it, but my nearest is 70 miles away, but I think it sounds just the job.
I am learning that all carbs are far from equal, not just in their raw state, but in the way they are managed e.g. very slow fermentation methods of production, and in the case of bread, the leavening method by which the natural yeasts are utilised from the grain surface. I am sorry to say that it has taken me to reach my late 60s to realise the attributes of food production as practiced in the past, and that have been so subliminally damaged during the last 50 years.
I don’t want to risk turning this fantastic blog into a cookery thing, but honestly, the health professionals ought to study food production during their course, and focus more on the human physiology so beautifully described by Dr K as above.
I wish!

I’m on your side in this Malcolm in that I’ve no doubt that carbs raise Trigs and LDL cholesterol. Shown going back to at least 1960. However, if your outline above is so, how do you have any LDL if you eat no carbs at all?

Once again a brilliant resume. I also note that there are MDs “listening” and agreeing! A major step forward.

Now regarding the VLDL (The BAD one) my own searching has lead to the following which may help in answering some points.

Re VLDL as I understand it is related to triglycerides and a rough measurement of it is approximately 1/5th of the triglycerides. VLDL is the small dense dangerous type B particle size of LDL cholesterol compared to the large fluffy relatively benign type A which is essential to the immune process against infections.

Thus a high LDL (fluffy) Type A is good while a high VLDL (Type B) is bad.
Saturated fat helps lower triglycerides and VLDL and increase HDL. The Trig;lyceride/HDL ratio should be <2
Two books (Cholesterol and Saturated Fat Prevent Heart Disease and Low Cholesterol Leads to an Early Death by David Evans) list some 200 refs on the subject.

Some relevant refs:

Circulation. 2000;102:1886-1892.
All factors, when elevated, (i)VLDL–apolipoprotein (apo)B100, (ii)VLDL cholesterol and (iii)apoC-III were associated with higher rates of heart disease.

The atherogenic lipoprotein phenotype is characterised by a moderate increase in plasma triglycerides, a decrease in high density lipoprotein cholesterol and the prevalence of smaller denser low density lipoprotein particles. The prevalence of this partially inheritable phenotype is approximately 30% and is a feature of the metabolic syndrome associated with an increased risk for cardiovascular events. The predominance of small dense LDL has been accepted as an emerging cardiovascular risk factor by the adult treatment panel (ATP) III.

Ever since I was diagnosed with type II and started a LCHF diet (which has gotten my A1c down to 4.5%), I have been told that a LCHF was not a good idea because of CVD. Even my wife was worried at first (she has mostly come around but still harbors doubts). We have all been brainwashed.

Another triumph of a blog, Dr Kendrick! How do we get the facts to the people who matter? To the “experts”, dieticians, doctors, government, the general public who have been conned for so long?
Keep writing, please…

HOW TRUE,, i love reading your blogs DR KENDRICK, they are such an insight how we are all driven like the proverbial ”lemmings” just because everyone else is going in that direction, probably why I have lost a few friends over the last few years of following your very ”WISE WORDS” . Thanks for the insight–‘the real deal’.

I realize I am late to this party, but please know there are a few of us who get it!
Actually, I got it when I was only a registered nurse, and lamented the damned diabetes drugs I doled out, while the patients ate processed crap! Now that I am also a clinical nutritionist, and specialize in low carb and ketogenic diets, I SEE insulin and HgA1c drop by removing most carbs. Very gratifying.

Fasting TGs can be up because your liver is processing extra fatty acids due to weight loss, so recycles and sends some back out. Non-fasting TGs will be relatively high because this includes chylomicrons after eating LCHF. CRP probably up due to heavy exercise if that’s part of your program. Hopefully your HDL is excellent and your LDL normal (i.e. “high”),

ASP promotes storage of fat in fat cells, insulin keeps it locked in there by inhibiting the disassembly of fat molecules (which are too big to get out).

I myself follow a keto diet (as strictly as I possibly can) and my weight loss is pretty much zero. I may have lost a bit of fat, but definitely not weight. I’ve also had to find out that I very easily gain weight just by overeating on “safe foods”, so the fat definitely gets tucked away without raised insulin. If it were any different, our species would’ve died out a long time ago.

Makes sense that carnivore mammals have to store fat for survival. Does this mean that body fat accumulation is essentially about “portion control” aka calorie-counting so that a nutritional intake surplus simply causes fat gain?

Or is the nature and make-up of the nutritional intake also important so that certain foods contribute more than others to fat accumulation despite being carb-free?

Well, carb free doesn’t mean insulin free. Protein stimulates insulin as well, which is normal, but to a lesser extent than carbs. According to Dr. Bernstein (quite famous DM doc) protein requires about 1/2 the insulin compared to barbs (when injected). The type of food does matter. It does matter what is consumed and of course how much, no way around that.

However, I don’t particularly like the phrase “portion control”, as it insinuates a conscious act, which is absolute nonsense! As Prof. Noakes has stated numerous times: “there are no fat lions”, nobody would even think that lions practice portion control, when hungry they eat until their bellies distend & fast until the next time. No lion knows about portion control, and even if they did, they wouldn’t give a rat’s arse about it. It’s all about eating when hungry, which is instinct behaviour.

Given that the body is fed with appropriate food, the subconscious is in full control of hunger, there will be no food cravings. I have experienced that myself. You could shove a piece of the tastiest cake into my mouth and I wouldn’t eat it unless painfully hungry, which never happens.

When I eat, I tend to shut off all thoughts about “portion control” or “is it time to eat” and let the lion do his thing, the lion only eats when hungry, no matter where I am and what time of day or night it happens to be. The only time I use my remaining intellectual faculties is when shopping for food, making sure I only buy food stuff that doesn’t mess with insulin levels and conjures up cravings. Once that is done I don’t need any self-control whatsoever, eating runs on auto-pilot, which is the way it’s supposed to be.

Ok. Great answer and very interesting. By the way Taubes quotes experiments in Germany pre-war where it was shown that removing micro-nutrients from diet triggered increased appetite in dogs(another layer of the appetite onion). I perfectly understand and make the argument that there is no obesity in the natural world (both human and animal) when I evangelize healthy eating.

I personally eat only when hungry and as a result generally eat once a day in the early evening. I am 66 and in superb health. My energy and focus is that of a young man. I have been a paleo eater for 15 years (used to be called Atkins).

You started to answer what I was actually trying to ask which is… As I contemplate my eating decisions (which are already healthy), if I wish to lose an inch or two from my waist (I have some clothing which would start to fit) how should I adjust my approach?

Based on your Lion analogy, eating to satiety and fasting would be ideal. But given that fasting routinely is not attractive, it looks like preferring fat over protein is a good start and limiting food intake could be good too?

The reward hypothesis does make a certain, completely unscientific, instinctive sense to me. But it should, because highly rewarding foods, moreish foods, are so often not real foods. I like salted cashews and I can just about get away with them in my relatively lchf diet. But you wont find them with salt on the trees! I try to eat them with other less “dangerous” foods, often other types of nuts, unsalted.
Fung agrees that low carbers only have half the picture, and that we should eat real food (surely all good diets involve eating unprocessed foods which dont have a long ingredients list?!) and fast sometimes.
Fung also points out that some high protein foods raise insulin more than some high carb foods, and thats why fasting is key. It is also why the emphasis is on high fat, not protein (and it never was, to those who read people like Atkins correctly) – lcHF…
What we call a low carb diet means we get rid of processed foods which combine unnatural, trans fat and sugar. So, it isnt sufficient to say we are eating more fat just that it is combined with carb, because the opposite is also true. It is misleading and contradictory.
In a world where there’s more obesity than ever, and obese people are often eating processed junk, a real food diet is relatively lchf. And relativity is key, especially if we belive that insulin makes you fat, insulin sensitivity is a continuum, and we need dietary fat, but not sugar.
And, if we don’t believe those things, “we” are wrong. Probably.

Great post. What is your take on increased LDL-C on LCHF diet. Some people including myself have seen dramatics rise in LDL-C after going low carb? Also, what are your thoughts on LDL-P as the driver of heart disease?

Good post but I think that you left out the classic study from Volek’s lab which showed that those who had been on a low carbohydrate diet had LOWER levels of saturated fat than those on an isocaloric low-fat diet even though the low-carbohydrate diet had three times the amount of saturated fat as the low-fat diet. I described it in blog post “Saturated Fat. On your Plate or in your Blood?” at http://wp.me/p16vK0-aY re-cycled in my book which I am trying to get printed in the UK.

I was just about to make this point. Not only does eating a high carbohydrate diet with no saturated fats result in an increase in saturated fatty acids in the blood (as you have shown), but the converse is true. Eating a low carbohydrate diet high in saturated fat results in a decrease of saturated fatty acids in the blood because as Dr Volek showed, saturated fats are preferentially oxidised.

It is literally the opposite of where your intuition would lead you, if you believe that you are what you eat. This is the reason why no one will see the emperor has no clothes.

rdfeinman, you are correct. I have had a lot of “experience” with the low fat and HFLC diets. I can tell you that the only one where I felt really good was the HFLC. Weight was good, all vitals perfect. I thought it rather odd that not many people believed in it. I actually tried to reduce the amount of fat straddling the fence, if you will. However, the lower the carbs (even those of the “healthy variety”) the better one feels. You have to watch those hidden ones. The only two people I knew who advocated this “diet” were Dr. Atkins, and later, those men who I knew in the U.S. who wrote a book (first edition 1993, I believe) called “Sugar Busters”. I literally could not put that book down. I had no idea how the glycemic index affected our metabolisms as we were so “saturated” (forgive the pun) with the notion that low fat was the bomb. It sure was nice not to have that fake butter in the house!!! Finally I gave up the old adage in dieting that did not work which said: “If it tastes good…spit it out!” What the heck? Buggars!!!

“Chylomicrons, however, do not convert to LDL and have nothing whatsoever to do with heart disease…”

Just a thought: It could be that LDL might go up in some people to replace cholesterol taken by postprandial chylomicrons. Besides possessing Apo A1, postprandial chylomicrons seem to be the most effective at cholesterol efflux – like a super-HDL.

“the thoracic duct. Which is a secret passage from the gut that opens out in one of the veins in your neck. ”

I learn something new on this blog every day! The trouble is, that from now on, when I eat saturated fat (which is more frequently than 5 years ago!) I fear I will imagine the stuff entering a vein in my neck shortly after! Presumably these are free fatty acids, not triglycerides by this point? Heck – it might get stuck somewhere!!

Your blog does a great job of reducing this nonsense to its absolute essence – which is great! Perhaps you should email a few prominent professors with a link to this piece, asking them if they would like to contribute a resolution to your paradox!

David, chylomicrons do not contain FFAs (or at least not many). Triglycerides are the preferred way to transport fatty acids round the body. When they leave lipoproteins they are turned into FFAs, absorbed, then reconstructed into triglycerides inside fat cells.

I think the brain makes some insulin, and absorbs some (less, not more, if hyperinsulinaemic) across the BBB for its own purposes, not necessarily the same as the body’s; this doesn’t affect glucose uptake but probably influences its disposition; in hyperinsulinaemia of T2D the brain gets too much glucose and not enough insulin to dispose of it properly – this is a factor in Alzheimers. Lower serum insulin – insulin sensitivity – means the amount of insulin getting into brain is optimal. At least, that’s how I read a confusing bunch of Alzheimers’ research.

This is one of the most understandable explanation of carbohydrate metabolism so far in my career. Dr. Kendrick makes it so simple often repeating the salient points so eloquently that even a 5 yr old can understand. Thanks doctor..😊😊

I just can’t understand their logic when it is also clear. No wonder these so called professors and nutritionists can t see that the emperor is not wearing his clothes because it Los like the blind leading the blind. I guess the cereal industry has a hand in this with their dubios and misleading advertising blitz. When I ask my patients to stop eating oat meal for breakfast the standard reply is”but doctor it is good for my cholesterol”. I persist with the same slogan of avoiding carbs and six months later they call recant….

I agree. I have followed Dr. Kendrick for a long time (well two years now) and read both books. I feel like a six year old…I have learned so much. But, not having an MD and having to try extra hard to understand these mechanisms and cell biology takes a while for us laypersons. I had forgotten all my statistics and Dr. Kendrick helped me to understand the math. By George I think it is coming together. I hope to reach seven years old next year. I mean that as a joke and compliment!!!

Thanks for this Dr Kendrick, nicely written. I was wondering if you had any thoughts on what is happening inside the minority of people who’s LDL does increase, sometimes dramatically, after venturing into LCHF (emphasis on SFA). Some type of problem with lipid metabolism? Or is it too complex to pin down? Cheers.

This is the first time in years of reading many, many blogs that someone has elucidated the processes so simply and magnificently. I hope your blog goes “viral”, so to speak, because we all know that there are way too many people reading and commenting on blogs who have no idea what they are talking about. And, unfortunately, something to which you already alluded, there are medical professionals among them.
I loved the blog. Thanks.

So, if someone eats no carbs at all, then they can never ever manufacture new LDL?

That seems unlikely to me.

It should be easy to verify though. There are quite a few zero-carbers out there, surely one of them had their LDL levels tested many times over the years. Anyone?

As an anecdote, my LDL was never as high as when I got tested after a one-week fast. I had not gotten tested right before the fast, so I can’t be sure that my LDL did not decrease over that week (to fit your theory), but it seems more likely to me that there is another way for the body to manufacture LDL, without any carbs.

Traditional Eskimos also have a low carb diet, eating mainly fish, whale, walrus etc. A group in Alaska were researched in 1972 and the researchers found that the incidence of heart disease among Point Hope residents was ten times lower than in the general Caucasian population of the United States.

Be aware that real measurements of LDL are fairly rare. In place the Friedewald formula is used to estimate the LDL value from the total cholesterol, the HDL and triglyceride. The problem, even if we bought into accuracy of the formula, is that it was calibrated on a sample of population that might not be representative (afaik it was calibrated on New Yorkers) and even then, the formula should only be applied if trigs are in the range of 100 to 400 mg/dl. But on low-carb, trigs go easily and quickly well below the 100 mg/dl limit, making the lab formula completely inappropriate.
Most MD and labs don’t know that.

Statistical analysis showed that when triglyceride is <100 mg/dL, calculated low- density lipoprotein cholesterol is significantly overestimated (average :12.17 mg/dL or 0.31 mmol/L), where as when triglyceride is between 150 and 300 mg/dL no significant difference between calculated and measured low-density lipoprotein cholesterol is observed. In patients with low serum triglyceride and undesirably high total cholesterol levels, Friedewald equation may overestimate low-density lipoprotein cholesterol concentration and it should be either directly assayed or be calculated by a modified Friedewald equation.

Gil it depends on you body and where you are metabolically speaking. Go on any site and research the glycemic index of these foods. Then set a goal for how many carbs you can or feel you need in a day. I always felt that if you ate fruit it should be that with a lot of fiber and should be consumed at least two hours from any sit down meal. I find that the most simple way of determining how to “manage” your metabolism.

I read history & politics & I was hopeless at all science related matters at school. However, I ploughed my way through Gary Taubes’s epic tome Good Calories Bad Calories, making notes in the side lines, checking things, back-tracking, re-reading to make sense of the science behind how bad carbs are for us. Having been aware that low-carb high-fat made me lose weight for years, but always dodging the brickbats from everyone about how it would give me a heart attack, high cholesterol, high blood pressure, ruin my kidneys etc – it was so great to be able to counter all that nonsense.

I love your explanation, really nice & straightforward. It will be added to be arsenal of counter attacks to all the low fat diehards!

Reblogged this on Now Have At It! and commented:
I have come to the realisation that I eat way too many carbs and not enough healthy fats. Could following a Keto way of eating help with that? I am still eating clean – only focusing on fish and veg plus less fruit. No major change in what I eat – just the way I eat it

“Studies reveal that many complex carbohydrates such as bread, rice, and potatoes have glycemic indices similar to or higher than simple carbohydrates such as sucrose” this from a study in 1984, so the science has been out there for a while. The powers that be just chose to ignore it.

I have asked a few doctors (GPs) there opinion about fats and carbs and I think there is a turning in thinking, as most now believe high carbs to be bad and fats not to be “too bad”. Progress?

How is it then, that some folk (eg Jimmy Moore and others) present with sky high LDL after going LCHF?

Dr. Malcolm Kendrick Post author
June 24, 2015 at 12:20 pm

Don’t know. But I do know that the Masai villagers of Kenya (traditional diet all meat, blood and milk and no vegetables) had very low LDL levels.

Doug:

By your explanation, the high LDL on HFLC should be impossible, but Chris Kresser once quoted something like 30% for the number of people who fall into that category. And add to that the LFHCers who seem to have low LDL.

Respectfully, doesn’t this suggest that your naturally very simplified description is missing something important? The theory doesn’t seem to match the observations.

Regular consumption of sugared beverages is associated with a greater prevalence of fatty liver disease, even after adjusting for body mass index, according to a large observational study.

Specifically, adults who drank more than one sugar-sweetened drink per day were 55% (95% confidence interval [CI], 1.03 – 2.35) more likely than nonconsumers to have nonalcoholic fatty liver disease in an analysis of data from the National Heart Lung and Blood Institute’s Framingham Heart Study’s Offspring and Third Generation cohorts. Jiantao Ma, PhD, from the USDA Human Nutrition Research Center on Aging at Tufts University in Boston, Massachusetts, and colleagues report the study findings in an article published online June 5 in the Journal of Hepatology.

The investigators analyzed data from questionnaires of 2634 predominantly white, middle-aged adults and categorized participants as either nonconsumers or consumers of sugared-sweetened beverages (SSBs) and diet sodas. Of the participants, 34% were nonconsumers and 12% were daily consumers of SSBs. Among SSB consumers, caffeinated cola consumption was the largest contributor to SSB intake (40%), followed by noncarbonated fruit drinks (29%), carbonated noncola beverages (21%), and caffeine-free cola (10%).

The authors found a dose-response relationship between SSB consumption and fatty liver disease in a multivariate analysis, adjusted for age, sex, alcohol and diet soda intake, and body mass index. Compared with nonconsumers and individuals who consumed less than 1 serving of SSBs per month, those who consumed less than 1 serving of SSBs per week (but more than 1 serving per month) had a 16% increase in risk (95% CI, 0.88 – 1.54). Those who consumed from 1 serving per week to less than 1 serving per day had a 32% increased risk (95% CI, 0.93 – 1.86), and those who consumed more than 1 serving daily had a 61% increase in risk (95% CI, 1.04 – 2.50; P for trend, .04).

Similarly, there was a dose-response relationship between SSB consumption and elevated ALT, with a 30% increased risk among those consuming more than 1 serving per day compared with the lowest consumers (P for trend = .002).

Although adjusting for body mass index did not attenuate the elevated risk for fatty liver disease among SSB consumers, SSB consumption was linked to the volume of fat in the liver among overweight and obese individuals. The authors did not see a similar association among normal-weight individuals.

The researchers did not find an association among diet soda intake and liver fat or ALT after adjusting for potential confounding variables, including body mass index.

The overall association between SSB consumption and liver fat was independent of body mass index and subcutaneous adipose tissue in the current study. However, the authors report, “further adjustment for VAT [visceral adipose tissue] attenuated the observed associations, suggesting that VAT may, in part, mediate this association.”

Although the specific effects of sugar intake on the development of fatty liver disease, particularly after long-term consumption, is not yet fully understood, “[t]he present study contributes to the existing literature by illustrating that regular consumption of SSB is associated with greater prevalence of fatty liver disease, particularly in overweight and obese individuals,” the authors write. “[P]rospective observational studies and controlled intervention studies are required to determine the independent association of excess SSB intake on liver fat accumulation.”

Funding for this study was provided by the National Heart Lung and Blood Institute’s Framingham Heart Study and the Boston University School of Medicine, and support from the US Department of Agriculture. The authors have disclosed no relevant financial relationships.

J Hepatol. Published online June 5, 2015. Abstract

As I said, if you have too much sugar in your body, where does it go? Once you have stored 1,500 calories it can go to only one place, the liver. Once in the liver only one thing can happen to it – conversion to fat. No other fate is metabolically possible. What is missing? That sugar is turned into…..what? There is nothing else for it to do, nowhere else for it to go. Ever looked at a Sumo wrestler? What do they eat? A low fat, high carbohydrate die, and people still believe that you can’t get fat from eating carbs? Ho hum.

I suspect that it is in the fractionation of LDL which can be high because of high levels of Type A ‘fluffy’ LDL essential for the immune process. For an estimate of VLDL (bad) Type B LDL, divide the triglycerides by 5. The NHS (at least locally) has yet to catch up with more recent research that shows that the trigs/HDL ratio should be <2. They totally ignore the Type A, Type B LDLs and their relevant imoportance. But then total LDL-C is the reason for must flog statins.

Doug
Indeed, while consuming a lot of fat and protein andd a little carb, my LDL upsets the hospital experts (not my GP – another Kendrick fan). However the triglycerides are low and HDL reasonable so that if one subtracts VLDL estimate (trigs/5) I have a lot of Type A, AND I haven’t had a “flu” infection in 5+ years.

Have to wonder about step 9 “As can be seen, the only source of LDL is VLDL.” I have an extremely low carbohydrate diet, by that I mean around 30g carbs per day, they are from the small amount in leafy green veggies, a bit in milk in my tea and coffee, and some carbs in almonds. The rest of my diet is high fat with moderate protein. No hidden carbs, no starchy carbs no sugars zero. I’ve been eating this way for the past eight years or so. My cholesterol levels have risen, my total is around 7.5, my HDL is around 3.5 but my triglercide levels are normally around 0.5 which is a reflection of my low carb diet, of course my LDL is high even using the Iranian forumla to calculate it. So your saying that the only source of LDL is VLDL which is from carbs doesn’t make a lot of sense to me……..

I did not actually say that. I did say that the only source of LDL is VLDL. The only source of VLDL is not carbs. But if you eat a high carb diet, the liver converts the sugar to fat and the only way to get that out of the liver is inside VLDL ApoB-100 (alongside cholesterol). The liver will resorb chylomicron remnants and Apo B32 VLDL and gets hold of (some) fat that way. [Yes, sorry, there is another form of VLDL, that does not become LDL. Hey, I never said it wasn’t complicated].

I did not actually say that. I did say that the only source of LDL is VLDL. The only source of VLDL is not carbs. But if you eat a high carb diet, the liver converts the sugar to fat and the only way to get that out of the liver is inside VLDL ApoB-100 (alongside cholesterol). The liver will resorb chylomicron remnants and Apo B32 VLDL and gets hold of (some) fat that way. [Yes, sorry, there is another form of VLDL, that does not become LDL. Hey, I never said it wasn’t complicated].

Oh, I misunderstood your post then, sorry. I’m happy with my ‘high’ LDL though…I mean according to Dr Ravnskov LDL is protective against infection. And with my lipid profile I should have the large fluffy kind of LDL anyway.

Some (a minority) of very low carbers, eating close to zero carbs but tons of saturated fat, do seem to get very high LDL. I have experienced this myself. Peter Attia has written about it (though he focusses on LDL-P rather than LDL-C). Peter has found that some people have to reduce saturated fat consumption to get LDL down. Would be curious to hear what you think the mechanism here might be—a separate question of course from whether or not Peter is right to worry about this.

You don’t have to get LDL down, whatever the latest fashion for the specific subtype may be. The smaller dense LDL (if it truly exists) is usually associated with insulin resistance, high VLDLs and low HDLs. As for LDL-P. Yet another adaptation of the hypothesis. How many ways can the cholesterol hypothesis be changed and adapted in a desperate attempt to make the facts fit the hypothesis. It seems there is no limit.

Interesting to me that Peter Attia, seemingly quite a smart, open-minded fellow and an advocate of LCHF, seems utterly convinced of the LDL-P hypothesis. Seems to believe it’s essentially proven now, along with the clinical benefits of lowering it when elevated. Dr. Dayspring’s influence, perhaps.

He cites his evidence in his “Straight Dope on Cholesterol” series of blog posts, especially from Part IV on: eatingacademy.com/category/cholesterol-2. Maybe I’m thick, but I still don’t see proof here, just, mostly, more correlations that could mean many things. Stronger correlations with disease than LDL-C and the other previous bogeymen at least, but what do they really mean?

Reblogged this on Ian's Health and commented:
Interesting article from Dr. Malcolm Kendrick here, explaining the digestion pathway of carbs and it’s significance in relation to heart disease and cholesterol.

Hi Dr Kendrick
Your diet is typical of that followed by my mother who survived into her 105th year and lived independently until well over the age of 100.
Thanks for carrying the torch, long may you keep it alight.

Why Dr. Kendrick, one would think you live in a Five Star hotel. Bully for you!!! Glad you don’t spit it out if it tastes good!!! Great come back I might add. Enjoy life. Laugh. Make us laugh.
If they dance on your grave, you won’t even give a hoot!!! Thanks

Hi, I am on a keto diet and found this post very helpful! I love that it is explained in simple steps that anyone can understand. Finally I have a great argument I can use without stuttering, when someone tells me I will die from all that fat 🙂

Now I know how carbs behave when eaten, but I still don’t really understand what happens when you eat fat.
Is all of it used as energy?
What happens with the excess fat you eat and don’t use up.
Why do some foods spike insulin levels even when they have no/very low carbs?
What happens in the body which has elevated insulin levels, but no carbs to convert to fat?

I’ll be glad to read any clarification on these question, or be directed to some useful sources. Thank you!

> What happens with the excess fat you eat and don’t use up.
If it is absorbed in the gut, it makes you fatter! If you don’t absorb it for some reason, you’ll find it in the loo.

> What happens in the body which has elevated insulin levels, but no carbs to
> convert to fat?
Elevated insulin is very effective at blocking the release of fat from the fat-cells, it makes you fatter & keeps you fat. If you have elevated insulin (more or less implies high-ish carb diet) and the body runs low on carbs (say a missed meal), blood glucose might drop & you’ll end up being hangry: “give me food NOW, or I’ll bite your head off!”.

It is a given that a calorie surplus on cellular level creates body mass, definitely when a lot of insulin is around.

The notion of “calorie counting” assumes that the properly-fed body is too stupid to regulate itself, which is nonsense!

You only have to calorie count / starve yourself / exercise 6 hours a day if you feed the body with inappropriate & addictive stuff. For a lot of people that is high-carb processed foods. Try overeating on steak + butter, good luck with that. Try it with chocolate chip cookies and pies and you’ll succeed.

There is NO mechanism in the body to store dietary food fat as body fat, the primary metabolic pathway of dietary fat eaten by its self or with protein SEPARATELY WITHOUT CARBS is beta oxidation or is used for body structure, hormone and enzyme production or is EXCRETED if not required.

I think one problem here is an old one — looking at one aspect of a system in isolation, which causes people to jump to certain easy conclusions. I agree with your observations about the lack of connection between saturated fat and heart disease. However, I’m going to relate my own story that might contradict those “easy conclusions” that I’m seeing in the comments.
Several years ago I went on a low carb high fat diet because I thought I was becoming diabetic. It went well the first few months — I felt way more relaxed than I normally do (I tend to be a “type A” personality). However, as time went on, certain things happened. I was constantly tired, sleeping 11 to 12 hours each night, and yawning many times in a row during the day. My hands and feet were constantly cold, even in the summer, even with several pairs of socks on my feet. And my cholesterol and LDL numbers went into the stratosphere. End result was a visit to the Emergency Room with a case of angina, with a doctor convincing me to have a stent put in.
Now, I’m not necessarily contradicting what you are saying in this article, just reminding everyone that there is a lot more to health than eating carbs or not eating carbs. And I have to say, I’ve never read any convincing evidence on what causes insulin resistance or type 2 diabetes. I’ve gone back to eating sugars and starches without guilt and feel much better.

Thank you for that insight. I would hope I do not come across as anti-carb fanatic. I do, however, feel there is a need to counter the absolute low fat high carb dogma that has ruled the world for the last twenty or thirty years. I do not think there is any doubt that, for the vast majority, less carbs would be healthier. And as for people with insulin resistance, carbs need to be restricted. yet the current advice is to restrict fat and eat carbs…. which is just total nonsense and potentially very damaging indeed.

But yes, one size does not fit all, and we must always be aware of that.

I find myself confronted with a glaring example of the unfortunate emphasis on carbs in the mainstream dietary world.
Since my diabetic husband entered a nursing home a couple of years ago, I’ve dutifully filled out his weekly menu packets, trying to make choices that minimize the carb load. But due to a recent foot injury, I was unable to visit for a couple of weeks. When I returned, I found that the dietary department had been completing his menus. Now when his dinner tray arrives, I see a carb festival: pasta, bread, non-fat milk, a small container of “I Can’t Believe (anybody thinks) It’s … Butter” spread, and 3 (yes, three!!!) fruit servings. But no vegetables. And he assures me the same thing happens every day at lunch. I guess it’s time to have a heart to heart with the dietician.

I know that I keep banging on about the number of copies of the AMY1 allele that individuals may have, but is it not possible that those who cannot ‘thrive’ on a very low carb diet are those with a large number of copies?
It may be that simply screening for the AMY1 allele count would give individuals the ‘power’ to find a diet that suits their metabolism.
At the present we are shooting in the dark a bit don’t you think?

That LDL comes from VLDL is simply a fact. It is of course interesting to ask why VLDL levels can skyrocket after a high carb meal, yet LDL levels stay exactly, and precisely, the same. Someone care to comment on that?

Well, of course there’s the “it turns into fairies” hypothesis, but I have my doubts.

It is more likely that it is regulated via some form of negative feedback. I am quite certain that there is not a single thing in the body that is not regulated, be it blood pH, temperature, electrolytes, blood glucose… some parameters have more wiggle-room than others. Compared to say blood pH or body temperature blood lipids seem to have quite a large range without any acute issues. Why? It probably boils down to how strong the influence of some value is on cell metabolism and how expensive it is to pull stuff in or keep stuff out. High blood glucose kills cells with GLUT1 transporters (not insulin modulated), so blood glucose has to be limited no matter what. On the other hand, cells can chose to express more or less LDL receptors & absorb what they need, if & when they need it (unless they’re forced to gobble up LDL by some news meds). So one could hazard a guess that lipid levels might not have to be as tightly controlled as glucose. Of course there are probably 100s of reasons why this might be wrong.

Anyhow… If parameters could go up or down as they pleased, chaos would reign, quickly followed by death.

But you’ve said it again Dr kendrick: “LDL comes from VLDL is simply a fact”. So someone, like me, on an extremely low carb diet who can’t be geting much VLDL, and I know it’s not because my trigs are always low, has high LDL (like Dan). So where does our LDL come from ?

From what you have already said, it sounds as if the requirement for triglycerides from VLDLs is fixed regardless of how many VLDLs are in one’s system. In any individual there are just so many sites where a VLDL can offload triglycerides and ‘become’ a LDL.

One thing that has to be kept in mind here is that LDL is not the same as LDL cholesterol. We usually don’t assess LDL cholesterol following a meal because the calculation of LDL cholesterol is partly based on triglyceride (TG) levels. As TG’s go up following a meal, the calculation of LDL cholesterol will be unreliable. So, a fasting blood sample is needed for calculation of LDL cholesterol.

“It is of course interesting to ask why VLDL levels can skyrocket after a high carb meal, yet LDL levels stay exactly, and precisely, the same. Someone care to comment on that?”

The conversion of VLDL to LDL is dependent on the action of lipoprotein lipase. This is a rate limiting step.

Lipoprotein lipase catalyzes the breakdown of VLDL, releasing TG’s for energy production or storage in adipose tissue. TG’s are moved from VLDL into LDL and HDL in exchange for cholesteryl ester. After the removal of TG’s from VLDL, the composition of the lipoprotein changes and it becomes intermediate-density lipoprotein (IDL). Later, when the amount of cholesterol increases, IDL becomes low-density lipoprotein (LDL).

The availability of LDL is determined by the balance between production and clearance. Clearance of LDL is highly dependent on LDL-receptor function, Therefore LDL-receptor function is a strong determinant of LDL levels.

Interestingly, the association of VLDL with atherosclerotic disease is probably just as strong as LDL’s. Ok, I know many here don’t believe in the lipid hypothesis, but anyway, the association is a fact. Whether lipoproteins play a causative role or not is another debate.

I also think it’s important to understand that raised blood triglycerides following a meal (postprandial hypertriglyceridemia) are caused by chylomicrons while elevated fasting levels are due to high VLDL, often caused by excessive carbohydrate intake. Both these types of hypertriglyceridemia may contribute to atherosclerosis.

Sorry to labour this point Dr Kendrick, and please bear in mind that I don’t have a problem having high LDL..happy with it high. But I wrote:
“But you’ve said it again Dr Kendrick: “LDL comes from VLDL is simply a fact”. So someone, like me, on an extremely low carb diet who can’t be geting much VLDL, and I know it’s not because my trigs are always low, has high LDL (like Dan). So where does our LDL come from ?”

and you replied:
“Yes, but I have not said that VLDL can only come from eating carbs.”

But I don’t have high VLDL ! THAT IS if triglycerides are a measure of one’s VLDL (my trigs are 0.5 which I know is low).

Does this mean that a person can have low triglycerides but high VLDL ? And if so, how do we get our VLDL measured ? It’s not part of the lipid profile test.

” it is possible to estimate the amount of VLDL cholesterol by dividing the triglyceride value (in mmol/L) by 2.2.”

So that surely means that a person with low triglycerides will have low VLDL My tirgs are 0.5 which means an estimate of my VLDL gives a result of 0.2. So back to my original question – if a person’s VLDL is low, as mine would appear to be, then how is it that my LDL is ‘high’ (even though I don’t mind) – it’s 3.8 by Friedewald and 2.7 by Iranian.
Anne

Anne, I don’t think anyone knows the answers to your questions. Normally LDL-C north of 6 would be cause for concern even among cholesterol skeptics. But what does it mean combined with HDL-C > 2 and TG < 1? I don't think anyone knows. If you look at the study data, they don't study populations with whacky numbers like that. I'm no expert, but haven't seen a single credible hypothesis for why a certain percentage of LCHFers (like yourself) present with such unusual blood lipid profiles. Some have suggested LDL receptor down regulation due to reduced thyroid function from low carb, but I believe that applies at most to a limited subset of people.

Many physicians can be talked out of recommending statins if you suggest that the best indicator of risk based on the medical literature is TAG/HDL (of commonly measured parameters, correlates with small, dense LDL). Yours is 0.77 which is very good (cut-off for risk is generally considered above 3.5). I have limited sample but many physicians are not as enthused with statins as the medical and popular literature would suggest.

Thank you for your work in this area. Diet is a small part of a doctor’s world, so they’re usually not too precious about it. Diet is the whole world of a dietician, so they defend the status quo. If a dietician’s wrong about diet, what’s left for them? And they are very wrong.

I don’t live there, so that argument doesn’t help me too much. How about no sugar, hard work and thousands of years to adapt, assuming they really are healthy.

How could eating glucose be good for us? Doesn’t a ten fold increase in obesity and a nine fold increase in diabetes in thirty years say everything. Rich, what’s your explanation for that? I mean here, not in some far away place.

It’s always very difficult when someone brings up some population and says “what about them?”, and they don’t fit the rules you’re trying to defend. Personally, I find it difficult to compare two completely different cultures.

The whole “low fat diet” came about in part because Ancel Keys compared fat “intake” versus heart rate for a bunch of countries. Why did that comparison use diet as an indicator of the differences between countries, when there are innumerable differences? I’ll give you an example. I’m headed to Sweden to see my wife’s sister and her husband. Her husband gets seven WEEKS off, paid, this year. SEVEN WEEKS IN A ROW. I’m from the US. It’s incredibly difficult and very stressful for me to take 10 DAYS to go visit them — I have to work weekends before and after, work long days both before and after, etc. And I get a MAXIMUM of two weeks of vacation per year. Even if there are differences in diet between Sweden and the US, why is it diet and not time off/lower stress that causes the differences (I assume there are some) in heart disease between the two countries?

Going back to the original question, it depends on the population. Some people argue that Japan and China, where relatively large amounts of carbs (as a percentage of diet) were eaten, eat many fewer calories and much less sugar than say the US. There are probably a thousand additional factors (exercise, number of cars, type of work, etc.) we could quantify.

From my personal perspective, I saw how a high carbohydrate diet helped to kill my father. His blood sugar was out of control. I realized the same thing was happening to me. Low carb (and now intermittent fasting) has allowed me to get my blood sugar, hemoglobin A1c, insulin, and insulin resistance under control. And I’ve lost 40 pounds at the same time.

There is no doubt that some people can eat carbs. I was at a friend’s house the other day, and they served sugar-sweetened iced tea. I haven’t had a sugar-sweetened beverage (other than beer, which is essentially that, unfortunately) in decades. Yet they can drink those beverages — the whole family is thin — and I’d weigh 400 pounds if I did.

To me, it’s a moot point about other cultures, as the US is and has been experiencing an explosion in obesity. That obesity appears to be driven by carbs, in my opinion. The blame is placed on fat, but since I eat as much fat as possible every day and yet have lost weight, in my mind, the fat is not the problem. I also don’t believe in calories in/calories out, exercise for weight loss, we need to eat 5+ meals a day, etc. Once I realized when low carb made me feel better that everything I new about diet was wrong, I now question everything. And pretty much everything the “experts” tell us is wrong, in my opinion.

If they are healthy on their diet, whatever that diet is, then they are genetically adapted to be healthy on that diet.
The problems start when their diet is changed from that to which they are adapted.
The difficulty researchers have in unpicking this issue is that interbreeding – largely over the past century – has mixed up the settled gene-pools and it is no longer possible to find well adapted groups of people who are genetically ‘uncontaminated’.
Research into the number of copies of the AMY1 allele is predicated (I think) on the idea that the numbers of copies have been selected for by the diets that relatively isolated groups of people ate, probably for up to for tens of thousands of years. Those eating high carb diets have lots of copies, those eating low carb have few – the numbers of copies found in humans varies from 1 to 15 so far (and counting – early papers say 13 max later say 15). See e.g http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2377015/
This is likely to be just one of the factors that enable groups of individuals to be healthy on diets that other groups of individuals would be unhealthy on.

I think that scientists were far more clever before the invention of statistics
In one sense I agree with you but statistics is simply a tool; a useful one if used properly. Unfortunately it is very easy to thow in a lot of (irrelevant????) data into a statistical package, press the button and out pops a RESULT and a research report to add to the CV.

The problem is that far less thought is necessary and more “papers published” is the inducement.

But don’t blame the tool any more than blaming the car for motor accidents – it is the driver (or researcher) as the case may be.

I totally agree with you. When I used to teach some of my fellow post graduate colleagues how to do multiple regression analysis I used to tell them that they should always remember that doing regression analysis was not a substitute for thought – think first (have a theory to test), compute second and then think again.

That was forty years ago when University computer systems were basic, punch card systems, based on fortran or algol and took ages to get results. Regression was hard work then compared with today. The recent ease in computing has resulted in much more research work being produced. A lot of work we are surrounded by today is not done properly and may be unintentionally poor.

Statistics are a very useful tool if used properly. Someone used to being respectful with stats is careful because they know how easy it is to make mistakes and loose the argument. Being an old fashioned statistical prude (OFSP) by today’s standards helped me to say no to statins and BP drugs despite not understanding the medicine at the time.

Thank you very much indeed Dr K for this article and to those who have commented. This is very interesting very to me.

Pat
I go back even further. My university decided in its wisdom that vets should know about statistics too get their degree. That was in 1953 – the book -statisics for medicine by bradford-hill. The means of doing stats – the brunsviga or facit. Inverting a matrix was done by hand. Great fun but limited.

One thing that has to be kept in mind here is that LDL is not the same as LDL cholesterol. We usually don’t assess LDL cholesterol following a meal because the calculation of LDL cholesterol is partly based on triglyceride (TG) levels. As TG’s go up following a meal, the calculation of LDL cholesterol will be unreliable. So, a fasting blood sample is needed for calculation of LDL cholesterol.

“It is of course interesting to ask why VLDL levels can skyrocket after a high carb meal, yet LDL levels stay exactly, and precisely, the same. Someone care to comment on that?”

The conversion of VLDL to LDL is dependent on the action of lipoprotein lipase. This is a rate limiting step.

Lipoprotein lipase catalyzes the breakdown of VLDL, releasing TG’s for energy production or storage in adipose tissue. TG’s are moved from VLDL into LDL and HDL in exchange for cholesteryl ester. After the removal of TG’s from VLDL, the composition of the lipoprotein changes and it becomes intermediate-density lipoprotein (IDL). Later, when the amount of cholesterol increases, IDL becomes low-density lipoprotein (LDL).

The availability of LDL is determined by the balance between production and clearance. Clearance of LDL is highly dependent on LDL-receptor function, Therefore LDL-receptor function is a strong determinant of LDL levels.

Interestingly, the association of VLDL with atherosclerotic disease is probably just as strong as LDL’s. Ok, I know many here don’t believe in the lipid hypothesis, but anyway, the association is a fact. Whether lipoproteins play a causative role or not is another debate.

I also think it’s important to understand that raised blood triglycerides following a meal (postprandial hypertriglyceridemia) are caused by chylomicrons while elevated fasting levels are due to high VLDL, often caused by excessive carbohydrate intake. Both these types of hypertriglyceridemia may contribute to atherosclerosis.

You have written: “Professors, who shall be nameless, appear unable to admit how basic human physiology works.”

You then write: “However, once this limit is reached, the liver will turn the rest into fat.”

Yet this isn’t what happens. Frayn covers it nicely in Metabolic Regulation. In practice, apart from the most extreme circumstances, de novo lipogenesis is negligable and doesn’t contribute to obesity.

The excess carbohydrates and amino acids become the preferred energy fuel in preference to fat, and these fatty acids then become stored.

From memory I remember that in humans (not rodents) even fructose to excess only contributes to DNL in the liver to 5%.

I’ve heard some debate about the actual amounts processed through DNL; similarly there is debate about whether excess protein will over-produce glucose through gluconeogenesis. However it seems pretty uncontroversial that the body makes saturated fat from excess carbohydrate. And that’s the main point of this article: ‘why have we been subjected to so much propaganda about ingesting a substance that our body produces, by design’. The following recapitulates the good doctor’s summary of this process:
from http://themedicalbiochemistrypage.org/lipid-synthesis.php
“When glycogen stores are maximal in the liver, excess glucose is diverted into the lipid synthesis pathway. Glucose is catabolized to acetyl-CoA and the acetyl-CoA is used for de novo fatty acid synthesis. The fatty acids are then incorporated into triglycerides and exported from hepatocytes as very-low-density lipoproteins (see the Lipoproteins page for more details) and ultimately stored as triglycerides in adipose tissue. A diet rich in carbohydrates leads to stimulation of both the glycolytic and lipogenic pathways. Genes encoding glucokinase (GK) and liver pyruvate kinase (L-PK) of glycolysis and ATP-citrate lyase (ACLY), ACC1, and FAS of lipogenesis are regulated by modulation of their transcription rates. In addition, the enzymes encoded by these genes are subject to post-translational and allosteric regulation. These genes contain glucose- or carbohydrate-response elements (ChoREs) that are responsible for their transcriptional regulation.”

Nice diversion – does that mean that you aren’t able to answer the question? Have you not fallen foul of the same bad science that you are accusing others of?

DNL is the road less traveled. The excess is not “turned to fat”. In normal people it will be less than one percent. Under extreme fructose loading maybe 5%. To increase this percentage we need to ingest around 5-6,000 kcals of carbohydrate over our body’s TEE.

The excess becomes the preferred fuel source, therefore sparing fat from oxidisation. We therefore increase the volume of our adipose tissue as the redundant fatty acids become stored in our adipocytes.

It is certainly complicated. I have advised all my patients to look at and adopt a Paleo type of low carb, high fat diet over the last 3 years, and if possible, a ‘leangains’ version of that, by delaying breakfast for as long as possible. The results are that total cholesterol may go up or down, but the TG/HDL ratio ‘reverses’ in people with high TG/HDL ratios over a period of a couple of weeks.

Out of concern that I might be worsening their situation (foolish thinking in my early days on this) I got blood levels at 2 weeks, 6 weeks and 12 weeks. Curiously some, but not all people with metabolic syndrome (MetS), and non MetS obsese patients, had their triglyerides skyrocket in the first 6 weeks. Though I didn’t panic, I was very concerned at first. The pattern that emerged is that when the rapid fat loss starts, the TG elevates but by 12 weeks, more or less, the ratios normalize. My thinking it is the rapid transport of TG out of the stored fat that is doing this. I no longer worry about it and warn the patients that the TG/HDL ratio may worsen before it gets better. Thoughts, anyone?

While not following a strict ketogenic diet I consume as much saturateed fat as possible – a diet that would probably give most nutritionists a heart attack. My trig/HDL ratio is well less than 2; my total NHS LDL level is >4.0 mml/L and I haven’t had a “flu” infection for more than 5 years, despite grand children. Vaccined – yes – but before I always got “flu” despite vaccination. The “fluffy” Type A LDL perhaps?

Incidentally, having worked in close association with animal nutritionistss for many decades, high grain diets are used to fatten animals. Even done research on the effects of parasitic infectins on nutrition.
Also, working with animals does have advantage that studies can be very precisely controlled – diets based on dry matter, digestibilty, inputs and outputs measured etc. I am still wondering what the “details” published on food packets are based on; crude calrimmetric data or what. Asked the local NHS nutritionist – ddidn’t know what I was talking about..

Jennifer,
I agree with you – Type 2 was just coming appearing in medicine but if I remember aright, the screening test was a urine test which is pretty insensitive (ketosticks??) – still used on me (amongst all the other tests) but I have never been positive by that test.

Dr Willcourt, very good to see a doctor helping his patients in this way. What is your simple explanation of the benefits of a low carb diet to a new patient?

Here’s mine to friends and please feel free to criticise. Everyone is welcome to contribute, but please remember that I’m trying to keep it simple for Joe Public!

The carbs you eat are quickly converted into glucose and raise your blood sugar. Your body can’t tolerate more than four grams of sugar in your bloodstream and sends insulin to remove it. Insulin stores the removed sugar as fat. Eating carbs causes your blood sugar to fluctuate and this results in you feeling hungry. You eat more carbs and the cycle continues and the result is obesity!

Indeed it is! and lots of diabetes too! Something I never saw in training 60 years ago. Type 1 was known but rare – Kirk’s Diagnosis. “mellitus” and “insipidus” 4th edition publ. 1953 NO TYPE II – but now – fat pets.

Mike. Back in the 1960s we routinely screened all patients for glycosuria. We would not be looking for diabetes mellitus because by the very nature of the condition those patients would have been urgent admissions, presenting with a catastrophic and acute decline in health. Diabetes insipidis was a very rare admission, and once again, the name just serves to confuse the issue.
But there seemed to be a need to check cold admissions for what I can only describe as non-acute symptoms similar to those of poorly managed ‘type 1’s as they became known. Indeed, screening did pick up these chronic sufferers, and the term ‘senile onset diabetes’ was coined, possibly because it mainly presented in the elderly. Now we know that has caused much confusion over the years, and, indeed there has been an explosion of youngsters presenting with the condition, which is why we are all getting so uptight about the causes of the condition, now better termed ‘type 2’.
I can only come to the conclusion that ‘type 2’ was slowly beginning to present its ugly head from the 1950s, because the diet was changing for the worse. I understand that numbers of type1 remain fairly static, because, as I know you are fully aware, its cause is far from that which manifests as type 2. I suspect that type 2 may have existed since sugar became cheap and plentiful, but in the early days of NHS, keen medics were looking for causes of chronic illnesses that the general population just had to suffer, and ultimately die from, in previous years.
I think my old grandma probably fell into that category, having the most awful leg ulcers for over 20 years, and which she tended to herself until she died in the early 1960s. There was never any mention of diabetes because she was probably never checked out, living out in the sticks all her life.
The difference with type 2, unlike type 1, is that at best, it is reversible, and almost certainly manageable, if only the medics would get their act together and understand that pills are not the be-all and end-all of coping with it. And the medics would stand a better chance of achieving a good outcome for their patients if they took control and refrained from sending their patients to diabetic nurses and dieticians!

What happens to the carbs? Interesting question; why they all turn to fat of course! I used to believe that but now I’m not sure. It depends entirely on context. It depends on your insulin sensitivity and what you eat them with. Clearly de-novo lipogenesis is an important mechanism though I think it is only relevant in the context of insulin resistance. I have started to really question the low carb paradigm and feel that it only explains half of the problem.

Lots of people around the world and throughout history have eaten plenty of carbs and have had no issue at all with obesity, diabetes and ischaemic heart disease. Why is that people who live in the ‘Blue Zones’ i.e. Okinawans, Kitavans and the majority of surviving hunter gatherer societies eat over 70-80% carbs and do absolutely fine.

What happens when you eat mainly carbs in the form of starchy tubers, fruit and dare I say it grains with minimal amounts of fat? Nothing earth shattering; they get broken down to glucose which then gets shuttled into cells and then oxidised to form lots of lovely ATP and intracellular CO2, any spare glucose then accumulates in form of muscle and liver glygogen. The latter is essential for all sorts of hepatic mechanisms not least conversion of T4 to T3 which is pretty important in supporting metabolism and hormone formation.

If you remain insulin sensitive, by keeping active, avoiding sitting too much, avoiding stress, getting plenty of sunlight and plenty of decent sleep you shouldn’t run into problems. In the context of a high carb diet you have to eat an awful lot of them before you start making fat and if you do at least you start making the healthy stuff (saturated fat).

When it starts to go pear shaped is when you add fat to the mix. When your body is faced with the combination of fat and carbs it going to use the carbs first and then store the fat; it is far easier to shuttle the preformed fat to adipose tissue than go through the palava of converting the carbs to fat and then oxidising the preformed fat. Is this a problem? Maybe , maybe not, probably okay if the carbs are coated in lovely butter or served with a juicy steak but will be more of a more of a problem they are coated or fried in easily oxidised omega 6 poly unsaturated fats.

If one persistently over eats it is the fat that makes you fat (sorry Gary) Over time this will produce a situation of excess cellular energy and muscle cells and more importantly adipose cells will be full to the gunnels with energy. Insulin levels have to rise to stop the fatty acids spilling out and causing significant damage ( remember in type one diabetes, its the increase in fatty acid levels that is much more dangerous than the hyperglycaemia). The fatter you get the higher insulin has to rise to compensate and the more insulin resistant you become. To prevent significant hyperglycaemia your liver has to act and this is where de-novo lipogenesis kicks in, after all, the glucose has to go somewhere and the least harm it can do is live the rest of its life out as palmitic acid.

This is pretty much the narrative of the of the last 30 years even the last century, yes the official guidance was for a low fat diet but nobody really paid that much attention and in actual fact in the west is the consumption of fat, mainly omega 6 PUFAS that has increased ,not carbs though it has been ‘hiding’ in ‘refined carbs’ i.e. chips, crisps, donuts pastries etc.

One is then faced with a problem, what to do next? Clearly one solution which is effective is to go low carb which a lot of people here have found effective . If you can’t process the carbs properly i.e. oxidise them and all that happens to them is get converted to fat then perhaps it is best to avoid them all together, though is it the best strategy? Clearly lots of people have found the opposing strategy successful by going ultra low fat and vegan zealots have claimed to reverse their diabetes and improve their insulin resistance eating food that a lot of folks here would shun like the plague.

The problem with going low carb is that that your body does actually need glucose and if you are not going to eat it you will have to get it from somewhere either from dietary protein or you will have to harvest your own protein via increasing cortisol levels and thats not going to be too healthy in the long term. The other issue is by eating higher up the food chain and eating mainly meat and dairy you have to pay really close attention to what you eat ate and that can be really tough, pork and chicken are probably riddled with too much PUFA and while red meat especially grass fed is probably safe from a fat point of view, you may have to be careful with the iron content. Check this blog for the role of iron overload in modern disease, fascinating stuff reetheanimal.com/2015/06/enrichment-theory-everything.html

It seems to me that this whole subject is soaked with cognitive dissonance on both sides of the fence. On the one side is the conventional view that carbs are good and saturated fat is bad, but fails to acknowledge consequence of eating them to excess is production of the food they most fear and the low carb camp, sat fat good ,carbs bad who fail to appreciate that carbs are potentially the cleanest source of saturated fat.

I hope I don’t ruffle too many feathers,but it is fun to challenge ones assumptions and dogma. I’ve just finished reading ‘The low carb myth’ by Ari Whitten and Wade Smith and recommend this if you fancy another perspective on this subject.

An interesting post. However, I shall repeat that you can only store 1,500 calories of glucose (primarily as glycogen), after that you MUST convert the excess to fat. If you do not believe this then please tell me, exactly, where the excess glucose/fructose goes? By excess I mean, over and above that required for energy generation.

Malcom,
I have no argument with you on this point as you say there are no carb pixies at the bottom of the garden to take the excess carbs way but neither are there calorie fairies that take the fat calories away. Calories still do matter. However there are carbs and there are carbs. Some are easy to gain fat on and others not so.

By my reckoning :

Liver Glygogen is around 100-120 grams
Muscle glycogen is around 500grams
Total body glycogen around 600grams or around 2400calories or about a days worth of food.

Without even dipping into this store the avarage energy intake for a sedentary male is around 2500cals.

If one were to eat a 80% carb diet this would mean you would have to eat about 1900 calories of carbs, or to put it another way a whopping 490 grams of carbs a day. Potatoes by weight are 20% carbs , whole fruit anywhere between 10- 25% carbs. This means if one were to eat only potatoes that would mean eating around 2.5kg in a day and thats just for maintenance!

Sounds crazy and probably not recommended or enjoyable but this guy managed it http://www.20potatoesaday.com. He ate 3 kilos of potatoes every day for 60 days and managed to loose 20ibs, improve his fasting glucose and improve his lipids.

Alternatively, if you have a sweeter tooth 490 grams of carbs would equal 18 bananas (about 2kg) or 23 apples a day ( about 3.5kg). Again not really recommended but my point is if you are eating carbs from natural sources it would be incredibly difficult to even eat to maintain body weight let alone trigger DNL and get fat.

However, imagine a 14 inch dominos pizza weighing at just under 900 grams . This contains 300 grams of carbs but because of the added fat (around 75) and protein (98g) will set you back 2290 calories, nearly a days worth in one sitting! Well it might be difficult to eat in one go but it would not sustain you for a day, the food reward is just too great, you will then eat to calorific excess and the excess fat gets stored as fat and the excess carbs get stored as fat.

Can eating refined sugar make you fat? Maybe not. In the 1930s back in the days when proper scientist did proper empirical experiments one researcher spent 6 months eating an ultra low (2%) fat diet and thrived, each day he lived on 4 pints of skimmed milk about 150g cottage cheese some potato starch biscuits and about 270g of sugar, drank as a syrup through out the day and half an orange and some vitamins for good measure. He lost 6 kg, felt full of energy all day never had a cold, his migraines disappeared and his BP improved.

Heres the paperhttp://jn.nutrition.org/content/16/6/511.full.pdf

Why is it you can loose weight eating lots of carbs whether it starch or sucrose but gain weight eating pizza? Two words; food reward, starch by itself , sugar by its self and fat by its self are not particularly rewarding for the palate but mix them together add some salt and other flavourings and you have a recipe for gluttony, calorie excess fat gain and DNL.

My dissertation tutor back when I was in medical school was a professor of physiology and an obesity researcher who made a name for himself by discovering a way to make rats fat. Instead of trying to force rats to eat regular chow he just gave them processed food, a ‘canteen diet’ all of a sudden the rats gorged themselves driven by food reward and then became obese. I think the concept of food reward is a concept that seems to get over looked but explains an awful lot.

We all know saturated fat isn’t evil or dangerous and we should know better than to start labelling other foods as evil or dangerous as well. Fat is fine, carbs are fine even sugar is ok. Its when we start to mix them up too much that things start to go pear shaped. We’re just very clever monkeys who have very unwisely altered our environment and now we are reaping the rewards for this manufactured mismatch with our biology.

DBM thanks for that post, very informative. I don’t think there is a single true path to weight loss, or certainly to weight gain. But most people will find it easier to lose weight eating fat, than carbs.

Thankyou. Theres no doubt that going low carb is a helpful and an effective tool for weight loss. I know this from experience but I’ve come to realise that it works for reasons other than we think it does. i.e. Its not through keeping insulin levels suppressed by avoiding carbs, it can’t be as protein and especially dairy spike insulin just as high if not higher than carbs.

Low carb diets work because of the lower, unforced, calorie consumption driven though the lower food reward of the diet which naturally leads you to eating less over all. Also the increased protein intake helps. My concern for low carb diets are the negative consequences for adopting this long term namely unnecessary and potentially harmful exposure to PUFAs and iron overload:

One of my over-riding concerns about the entire dietary debate is that there appears to be evidence of harm from every single foodstuff we can consume. I don’t like the idea that we view food as ‘the enemy’ to be conquered. If the Blue Zones proved one thing – to me – it is that a whole series of different diets seems compatible with long life.

Is it possible to simply excrete calories? Obviously those with diabetes excrete at least some in the form of glucose in the urine, but is it possible that some calories are just never absorbed at all?

Yes. Latest drug for diabetes is one which stops the kidneys re-absorbing glucose to it is simply pissed away. I don’t like this idea much. Certain foods, fibre, some nuts, a bit of this and that can simply pass through. The body is usually pretty good at grabbing food and clinging onto it though

“Why is that people who live in the ‘Blue Zones’ i.e. Okinawans, Kitavans and the majority of surviving hunter gatherer societies eat over 70-80% carbs and do absolutely fine. ”

That is a good point, and it does remind one of Ancel Keys, in that it is always possible to advance an hypothesis if one ignores the contrary evidence!

On the other hand, I do wonder whether hunter gatherer societies eat enough to get into overload, and also whether they live long enough to encounter the diseases of later life.

Your post seems to make a strong case for a traditional diet – not pushing to either extreme (which is also the easiest diet to adopt). Of course, people trying to recover from disease – T2D or cancer – may actually need an extreme diet.

Part of the frustration with medical science is that there is so little debate between different points of view – because the orthodox side have let themselves be pushed into such an extreme position that all they seem to want to say is “Read the guidelines, and ye shall be saved!”

The Okinawans are the longest lived culture on earth having the highest proportion of centarians than anywhere else in the world.

Here are a few quotes from Staffan Lindebergs survey of the Kitavans

‘Despite a fair number of older residents, none of whom showed signs of dementia or poor memory, the only cases of sudden death the residents could recall were accidents such as drowning or falling from a coconut tree. Homicide also occured, often during conflicts over land or mates. Infections (primarily malaria), accidents, pregnancy complications, and old age were the dominant causes of death’

‘The oldest living person during the survey was a 96 year-old woman, and during a previous visit a vital 100 year-old man was interviewed.’

‘The elderly residents of Kitava generally remain quite active up until the very end, when they begin to suffer fatigue for a few days and then die from what appears to be an infection or some type of rapid degeneration. Although this is seen in western societies, it is relatively rare in elderly vital people. The quality of life among the oldest residents thus appeared to be good in the Trobriand Islands.’

‘The main results of the Kitava study, that there is no ischaemic heart disease (and no stroke, see Chapter 4.2), are unanimously confirmed by medical experts ‘

‘The residents of Kitava lived exclusively on root vegetables (yam, sweet potato, taro, tapioca), fruit (banana, papaya, pineapple, mango, guava, water melon, pumpkin), vegetables, fish and coconuts [27-29]. Less than 0.2% of the caloric intake came from Western food, such as edible fats, dairy products, sugar, cereals, and alcohol, compared with roughly 75% in Sweden [30]. The intake of vitamins, minerals and soluble fibre was therefore very high, while the total fat consumption was low, about 20 E% [28], as was the intake of salt (40-50 mmol Na/10 MJ compared with 100-250 in Sweden). Due to the high level of coconut consumption, saturated fat made up an equally large portion of the overall caloric intake as is the case in Sweden. However, lauric acid was the dominant dietary saturated fatty acid as opposed to palmitic acid in Sweden. Malnutrition and famine did not seem to occur.’

The Okinawans are not even the longest lived culture in Japan. That would be Nagano. The longest lived country on Earth is Andorra. Incidently the Okinawans were knows as the Pig Eaters for the high consumption of pork. It is said of them the only part of the pig they do not eat is the squeak. Always be careful when looking at stats on diet in various countries. No-one studies this area without going in without a whole pile of preconceptions.

A most interestiing view.……you do at least you start making the healthy stuff (saturated fat).
May I suggest that this whole issue is very, very cmplex and that research has tended to restrict itself to particular sections of the problem based on various “hypotheses” such as Keys’ views on carbs, Yudkins’ views on sucrose, various views on sundry fats, gluten etc. each with there own agenda.

One is minded of the adage “a little of what you fancy, does you good”, In short, excess of anything is apt to upset what is a very complex metabolism.

May I take this opportunity in thanking all contributors to this most interesting debate. It has ccertainly helped me. I shall be able to enjoy spuds with my dinner and fried bread with my eggs and bacon

There are several things which you don’t address in traditional societies. I think that one of the big ones is total energy consumption. A 6′ man in a cold climate needs far more calories than a 5’4″ man in a warm climate, but that doesn’t mean that the 6′ man can tolerate a substantially larger amount of blood sugar, or that he has a massively larger amount of storage for carbohydrate. Relatedly, hunter/gatherers are well known for the relatively little amount of work that they need to do in order to gather their food. In short, when comparing why modern industrialized westerners get fat to why people living traditional lifestyles outside of the west aren’t, I don’t think it is legitimate to neglect their total energy expenditure.

There is also the issue of timing. Very fibrous foods are known to release their macronutrients – including their glucose – slowly, meaning that it would be entering the bloodstream relatively slowly. Since no one in the west eats any meaningful amount of fiber in comparison to carb-heavy thin populations, this again makes direct comparison tenuous.

Finally, there is simply the issue of descent. There have been a lot of sub-populations of human beings with distinct characteristics, such as the way that people of European descent (plus a few other groups, IIRC) can process lactose as an adult. It is quite possible that people who are from populations that were selected for on their basis of tolerating a pure carb diet would do differently than people who were selected for on the basis of doing well eating raw seal, all of whom might be different from other populations that did well in, say, northern europe or the mountains of South America, etc. In short, I don’t see the evidence that people descended from distinct sub-populations who faced different selective pressures should have turned out to be identical in spite of the different selective pressures. It’s just possible that people are different enough that different things work for different people, and we each have to try different approaches and see what works for us.

Your point about populations is very pertinent, particularly in the context of metabolism, location, availability of different food types. The variables involved are extensive. Vitamin D is one example – white skin (nothern) allows maximum production while dark skins restrict production but protect from damage. Vitamin C is another (most mammals produce their own) but humans have to get it from food. Problems with Vit C tend to be in the High latitudes. A nice little story on the benefits of Vit C is as follows:

http://www.odt.co.nz/print/126632
but ignored by medics is interesting. In 2011-12 winter UK some 650 died of flu – could
they have been “saved”?
On the basis of Dr Kendrick’s views on saving lives this is truly about a life saved

But back to the complexity of humans and massive number of essential elements, molecules et al, unless all are covered I wonder at the value specifically directed research at one aspect be it carbs, fat, protein, individual vitamins etc unless everything else is covered.

Hmmm….I ate a very low fat, high carb diet and still gained weight. I think a lot of it has to do with how insulin resistant you can be, which may be determined by genetics. Also, on a low fat, high carb diet, someone like me has a horrible time. I was constantly hungry (thanks blood sugar + skyrocketing insulin), depressed, angry at times — It was horrible. (That’s looking back; at the time, I thought everything was OK.)

I think food timing (number of times you eat per day) has a lot to do with it. Consider the following discussion:

His argument is that we’ve gone from eating 2-3 meals per day to eating 5-6 meals per day. In my case, that was correct. I thought that eating 5-6 times per day was healthier than eating fewer times per day. Simply by skipping meals (sometimes all day), I’ve lost 15+ pounds (US), and did not change my diet (low carb, high fat), and eat as much as I want to eat, when I do eat. That is, the timing of meals is important.

To be honest with you, I think we really don’t know anything. It’s like heart disease — we really don’t know what causes it, and 50+ years of research has some clues but not a lot of actual theories that are 100% reliable. Pick any “risk factor” (LDL, LDL-P, obesity, you name it), and you can find studies indicating that risk factor is or is not correlated with heart disease. For instance, see:

Total cholesterol and LDL not predictive of coronary disease, but triglycerides/HDL is. Yikes! Yet one more thing to be concerned about.

It’s similar with nutrition and its complex relationship to diseases. We know overweight people are associated with diabetes and insulin resistance, but did gaining weight cause insulin resistance or did the insulin resistance cause weight gain? I think it’s the latter, but no one knows, and you can certainly find adherents to the other side.

Yup yup yup! I learned decades ago that I would crash both physically and mentally after a couple of hours, so if I went on a long walk I would carry sandwiches (slow carbs), chocolate, Kendal mint cake, coffee with sugar etc. (fast carbs) and carb up every couple of hours, not realising I was not just treating a hypo but overtreating it and triggering another one a couple of hours later.
Now I routinely go 6 – 8 hours and often longer without eating anything, and don’t lose energy. Eventually I might feel like I ought to eat something soon rather than the knawing hunger I used to get. Obviously I am genetically adapted to metabolise fats rather than carbs, like at best a large minority and at worst a majority of the population. If anyone had told me this 50+ years ago I might not have suffered so much

I am awaiting the download of Whitten’s book. It will be interesting to compare it with Taubes’, Grove’s, Briffa’s and Ravnakov’s books.

The pro-carb research reports that I have are somewhat flawed – abstract and results somewhat different!

……………..pork and chicken are probably riddled with too much PUFA – omega 6

The current advice is to eat chicken, red meat being bad???.

May I suggest that the problem with PUFAs in pigs and chickens is that they are fed rations containing high carbs supplemented by vegetable proteins and probably vegetable oils (high omega6) and seed extraction residues (again high omega6) – I suspect similar to the human “plate”. The same would apply to factory farmed beef; grass fed meat and milk, as you point out, are much better for you.

My own experience was that moving to the officially advised diet, my appetite increased as did my weight – result diabetes despite increased exercise. Now back to my normal weight – BMI 26-27 – overweight on a hifat reduced carb diet. Flegal of the US CDC has reported three times on overweight being associated with longer life span but totally ignored by nutritionists. Dr Kendrick has raised the same issue.

Also there was a massive study – WHO-EU-Monica study that looked at the national “availability/diet content” of some 40+ European countries and their associated CHD mortality rates. On the Keys line I regressed national CHD mortality rates against data for Carbs, fat and fruit&veg. Nationally, fat and fruit&veg were highly but NEGATIVELY associated with CHD mortality rates. Conversely, carbs were very highly and POSITIVELY associated with CHD mortality rates; as I remember there were some 10+ zeroes before the first significant number in the estimated probability.

I hope I don’t ruffle too many feathers, but it is fun to challenge ones assumptions and dogma.

I entirely agree with you. The establishment view has always to be challenged. That is a major reason that I find Dr Kendrick’s blogs so brilliant. They always challenge the “official, conflicted, politically acceptable” and often wrong view.

DBM
8. Decrease in the unsaturated fatty acids as a result of the low-fat regimen indicates the probability that even the normal adult human subject, like the rat, is unable to fabricate the highly unsaturated fatty acids, which should, there fore, be provided in the diet

Have the book. my usual practice is to look at the list of cited references. I find this a good indication of the “open” or “restricted” approach to the subject. No list but links to blogs (some with an obvious agenda), some references. Not helpful! I will have to read it.

Hmm. For ‘vegan’ athletes who are burning 2500-3000 calories a day, and eating only vegetables & fruits; based on your rationale if they eat more than 1500 calories over what they burn, then they are susceptible to increasing their VLDL, and in turn, LDL?

How does a Vegan athlete manage their food intake while keeping higher levels of LDL at bay?

All the above are tropical or sub-tropical with a very high content of saturated and/or monosaturate fats – all good. Peanut oil has a high level of omega6 which, though essential, is bad if the ratio of omega6 to omega3 >2-3, preferably 1::1

Thank you for this great post which is completely to my ‘taste’ as being a strong LCHF advocate, since sixth years now, during which time I have learnt much of what you mention here. Judging from the number of comments on this thread it is evidently a very strong general interest in the relation between carbs and health. As you point out I don’t think it is necessary to strictly avoid the carbs if you are not hit hard, as me and my wife, by the metabolic syndrome. By the way, in my eyes, it is more appropriate to call this syndrome the ‘insulin resistance syndrome’.

An eyeopener for me was the scientific journalist Gary Taube with his solid book “Good Calories & Bad Calories” where he advocates the ‘insulin hypothesis’ as the fundamental in an endocrinological explanation to why people get fat. This makes complete sense to me. In contrast there is the 100 year old official calorie counting ‘explanation’ to obesity which ‘happily’ refers to the “First Law of Thermodynamics”, a law which can not possibly be refuted by any sensible person. (Thermodynamics being my favourite subject among the natural sciences!) This law can actually not be an explanation at all but is just simply a tautological fact note and as such it can not possibly EXPLAIN anything about obesity.

Thus as a non-explaining ‘theory’ the calorie counting theory makes no sense to me, e.i. it is nonsense but is still the ground on which the whole official edifice is resting. We didn’t count a single calorie but still I lost, just by coincidence, 20 kg on LCHF in a couple of years while my wife lost 12 kg although we didn’t care about those ‘few’ extra kilos we carried when we for health reasons decided to go “Low Carb”.

With all official investment and careers in the ‘calorie counting’ nonsense it is no wonder that the resistance should be hard from the remaining official advocates and I note today a firing back on the LCHF-hypothesis which is today unquestionably gaining momentum due to all ‘success stories’ on weight loss. Vanity is a strong moving force!

Funny enough I have now been asked by a Swedish journal to review a book, “The Low Carb Myth”, which on the surface appears to be a strong counterattack on my present belief in the LCHF as a remedy for people hit by the metabolic syndrome.

(This link has been removed by me, so that no-one gets sued. You can find Amazon links in other posts, cheers)

Is anyone familiar with this book and have any ideas about it since I really don’t know how to approach it rather than from a more philosophical point of view?

Interesting that you bring this up as I have just finished this book. It’s a well written, fair and comprehensive critique of not just the low carb movement but of the diet industry in general. I advise you to read it with an open mind though because it certainly challenges a lot of tenants of the low carb dogma in quite convincing fashion. I’d be very interested in your take on it.

Just having a read now.
Since you have read it, could you comment on whether there is any discussion of the genetic and epigenetic differences between individuals and long time groups of individuals (Eskimo Massai etc) that throw a rather large spanner in any generalised dietary advice?
Thanks.

DBM, you say we needs glucose but we can make our own without eating carbs. When I look back a few centuries to, say, 1600, what carbs did we eat in Britain or in most of Europe? By modern standards it must have been a very low carb diet. There was no refined sugar, no potatoes, no pasta or rice. There would have been some bread, maybe some grains and a little fruit in summer. In historical terms even bread and grains are relatively late additions to our diet.

In short, whatever the variables, in Europe for most of human history we ate a low carb diet. If you accept that point, how can the low carb diet be anything other than healthy?

Goran and DBM.
Very interesting indeed.
I am reminded of Dr Lustig saying that even dog poo can be made palatable if enough sugar is added to it.
In other words….all sides can put up good arguments for and against any concept they hold close to their heart.
I choose to remain blinkered into believing that LCHF is the way for me to continue. But I am re-introducing grains into my diet now, so long as they are eaten in fermented form.
After all….I follow a LOW carb, not a NO carb regime, and it works wonderfully for me.
Each to his own, as they say.

The problem is that there are so many studies, they can be used to support any hypothesis, especially if you just ignore the studies that go against your hypothesis. (Heck this is how the low fat diet and the cholesterol hypotheses survive.)

Also, most of the studies aren’t well designed to test their hypotheses. For instance, Gary Taubes brought up a good point. Say you eat 2,000 calories a day, 50% carbs, so 1,000 calories a day by carbs. You go on a diet to 1,500 calories and now eat 750 calories in carbs. You lose weight. Do you lose weight because you decreased calories, decreased carbs, or both? If you believe the calories-in, calories-out hypothesis, it’s the reduction in calories. If you believe in low carb, it’s the reduction in carbs. Who is right?

Studies also aren’t tightly controlled. I believe it was the A to Z study that studied low fat, Mediterranean, and low carb. The low carb diet came out best in terms of weight loss, but everyone regained weight over time for all diets. Supposedly, the low carb participants started eating 200 grams of carbs per day after a while. That isn’t low carb anymore. How does one interpret these results? You can choose to interpret them according to your bias.

One negative thing the current low fat dogma has produced is that basically all the money given out for studies went to prove low carb was good. None of the money, until recently, went to test alternative hypotheses. Heck, the Atkins diet was “mass murder” according to some.

So, the only way to read a book like that and actually critique it is to read the studies referenced by the author for yourself and make up your own mind. What if the author uses studies to support his theories and you don’t believe the studies actually support those theories, what do you do?

Oops, I meant all the money for studies went for studies to prove the low FAT (NOT low carb) diet was good. One consequence of this is that there is a massive number of low fat studies and not nearly as many low carb studies.

I think your mistaken if you think that medieval peasants ate a low carb diet. According to this site http://jn.nutrition.org/content/16/6/511.full.pdf the average peasant would have eaten 370 to over 700 hundred grams of carbs a day in the form of oats, bread beer and beans. Medieval Europe was comprised mainly of serf s tilling the land for their masters if there was meat to be had it would have been eaten in the main by the ruling classes and only on special occasions would the serfs be able to have any.

Eskimos and Masi aside the vast majority of cultures worldwide, both agrarian and hunter gather do not and have not eaten a low carb diet.

I’m an intellectual property attorney in the US. In the US, that link might be problematic, as you appear to be able to page through the entire document. If you just replace that with a link to the book (e.g., on Amazon.com or elsewhere), it should be OK.

It’s the ability to read the entire book that’s troubling (I don’t believe anyone would actually do that — as the font is too small and if you blow it up, you can’t read much — but I guess it’s theoretically possible).

I am sorry if I have made something ‘illegal’ by this link but I think it was an ‘open access’ sort of thing. However, along the line I read somewhere that they suggested that the reader should support the authors by buying a paper copy from Amazon and I think I must do that before getting into any serious review process.

So far I have just browsed the “Low Carb Myth” but in comparison with the more ‘scientific’ attitude I find, to my taste, in the “Good Calories & Bad Calories” I already have a problem with the confirmative (dogmatic?) attitude which seems to prevail throughout the “Low Carb Myth”. To me this is not a serious attitude but rather seems intended to ‘impress’ on average readers.

As a researcher of natural sciences I have great problems when I encounter such an attitude and usually I can not make myself fulfilling the reading of such books. I have already got a number of such ‘unread’ books in my bookshelves. (The philosopher Hegel’s works typically belong to this category.) Science must be humble by definition. And in this context I wonder why the main author is showing a picture of his muscular torso at the end of the book? This does not add to my confidence in the intellectual qualities of the book.

Well, no-one is able to approach the world without prejudices (old Schopenhauer teaching) and I guess mine is a LCHF one given my family success here – evident cause and effect seems to produce diehard (biased?) adherents.

I realise that I will have problem reading all the pages in the book and I have already told the editor who asked me to review the book that the only way I probably could manage to accomplish the task is to put the book in a philosophical, historical context starting with my favourite Greek one, Xenophanes who impresses on me by, among other things, his saying.

Roughly:

“We will never know the truth and if we by coincidence would arrive at it we will not know that!”

Such a review could be an interesting exercise for me and hopefully some readers of my review.

The copyright notice is on page 3 of the book/pdf link. It definitely suggests to me that we (the general public) should be paying for this book before reading it, and that someone who bought it should not be giving it away for free. But my knowledge of copyright law would fit on a postage stamp with lots of room to spare.

Thank you for the link to the forum which tells me what I have now known for six years. The carb/no-carb issue is a very, very hot subject.

By practically ‘saving your live’, as a severely metabolically injured person (e.g. diabetic or with a heart disease), through adhering to the strict LCHF ‘religion’ it turns you into a weird person in our high carb infected world.

And when you actually turn down an offer of a delicious piece of cake, which happens all to often, without good reason you are actually insulting. In my own case I openly admit being an ‘alcoholic’ when it comes to cookies and that no-one will beat me in the life time contest but stopped the contest after my serious heart attack. Usually after having declared that they let me off the hook but I may have ruined the party. And of course the declaration is made only when people start insisting or teasing you – the best way is to quitely ‘sneak away’ from the cake unnoticed.

Facing the global obesity epidemic the winds seem finally today to be slowly turning. Funny that our very religious neighbours didn’t have any problems with our LCHF-attitude when inviting us for a dinner. They actually made the dinner into a great, 100 % strict LCHF event – we love them!

There are arguments for both sides.
You can live low carb or low fat, you certainly can’t eat both.
If you are insulin resistant, as are a high proportion of western civilization, carbs are poison. We have a disorder of carbohydrate metabolism. How difficult is that to comprehend?
There are a lucky few who can handle carbs. Low fat is easy for them. How incredibly lucky are they! But it is not so for a huge proportion of the population.
It isn’t that carbs are bad or fat is bad, it is just that different groups of people don’t have the metabolic ability to cope with certain food groups.
Why the hell there is so much argument about this is beyond me. If you can’t metabolically manage carbs, so avoid them. It is obvious!
If you can live with low fat/high carb you have my envy. It would kill/disable me!

Liz, you are correct. All the scientific research in the world will never manage to explain each individual’s physiological mechanisms…..yes, there are traits that describe skinny families, and fatty families…..but then sometimes even siblings respond differently to the same meals put down to them.
I blame the over mechanisation of raw food materials e.g. to extract oils etc, and the introduction of sinister additives to extend shelf life.
60 years ago I recall asking my Dad if we eat to live, or live to eat.
He said he would tell me when I was a big girl; he died when I was 30, and never saw me as a big girl……because I remained slim until my mid fifties, after a couple of decades of modern food interference and inappropriate dietary advice splurted out by nutty dieticians.
Oh that Dad were here today…..he would have known the answers….because I recall him chuntering on about the demise of proper bread, the chemicalisation of the beer industry, the artificial colours used in confectionary, the contamination of fresh produce with pesticides, the homogenisation of quality milk. He knew instinctively all was not right with our food…..and as lad who left elementary school without a certificate to his name, he had more knowledge in his little finger than many of today’s academics.
As keeps being pointed out on this blog over the last couple of years, the knowledge is there, but it is a political/ big business problem!

Carbs are very “moreish” and that is their problem. And one has only to look at the shelf space in grocery stores/supermarkets to see what is popular. And they are there because people buy them.. Surely there is an association to obesity whatever the claims of nutritionists say.

And consumption of both refined grains and sugars increased by huge amounts on top of our already high-fat diets (AK).

However, this does not—as they try to imply—mean that our actual fat consumption went down. What actually happened is that overall calories in the diet increased (AK) (by about 350 calories per day since 1970), and the additional calories were primarily from refined grain and sugar products. Hence, the percentage of fat of the total calories decreased, but our actual fat consumption stayed just as high as it was before (ref: http://wholehealthsource.blogspot.com/2012/09/more-thoughts-on-macronutrient-trends.html ) a blog and difficult to identify where the data can actually be found.

My query:
The overall calories increase in the diet AK was 350 cal per day. This is equivalent to 127750 cal or 127.75 per annum. Thus by the year 2000 the diet has INCREASED to 3,832,500 cal or 3,832.5 Kcal – a massive 3,800+ nutritional calories and this on top of the BK diet and these Kcals were from “the additional calories were primarily from refined grain and sugar products”.

It seems to me that this shows that the obesity epidemic is due to a massively increased carbohydrate intake as the “actual fat consumption stayed just as high as it was before (BK)” though it is also admitted that “ the use of vegetable oils and trans fats (bad) skyrocketed (AK) so the contribution of saturated fats must have gone down.

Dr. Kendrick,
It’s a small point, but VLDL isn’t the only source for LDL, nor is LDL the only destination for VLDL. My reading of it is that the evidence is that in humans LDL is the predominant end of VLDL, but not literally the exclusive end of it. Also, VLDL is turned into LDL in the liver, since LDL and VLDL can be distinguished by their apoproteins (and, I believe, cholesterol content). I don’t believe that this affects your argument substantially, but since my wife objected when I showed her this article, I mention it as including that information may make it more persuasive. My source is this 1984 paper in the journal of lipid research: http://www.jlr.org/content/25/13/1570.full.pdf

I did answer this question in response to someone else. I eat what I like, I eat carbs fat, protein. But I usually call them steak and chips and salad – or suchlike. My view is that good food is delicious, one of life’s great pleasures, and should be enjoyed. I feel sorry for those with gluten intolerance, or carb intolerance. If I want to lose weight (which I possibly should at present, I go low carb, and it works for me).

Yep, good food is good food for me, as long as it contains less than 5-10g carb per meal.
Steak and chips, Sure! just don’t give me the chips, I love, love them, but they raise my HbA1c to unacceptable levels! In 10 years I would be blind, have my feet amputated, a stroke, myocardial infarction!
I don’t like steak, I like the chips.
So what is good food Dr K? Can it be defined for everyone?
Everyone is different. And I would say I am in the majority. An incredibly high proportion of the population cannot metabolically cope with carbs.

If I want a healthy old age I can’t have chips.

Dr K., I suspect from your history that you have a degree of carb intolerance.
You are chubby, you have a problem you are not addressing.

I can’t cope with carbs but the only carbs I eat are green leafy veg, almonds and some dairy, plus a glass of wine in the evening. I don’t ever miss the other carbs and it’s been nearly eight years I haven’t had them. I love steak ! Rib-eye steak with the fat, organically reared and grass fed cattle, full of flavour. And lamb. I also love sausages, as in a previous post by Dr K, saussices fraîche which are pure pork with no rusk or additives….can’t get them in England unfortunately but I crave them, especially as I’m now thinking about them as I write. I like veggies too: kale, courgettes, asparagus, brocolli and more, cook ’em in coconut oil and they’re so yum. And fish, good fresh fish, especially grilled sardines. And goat’s cheese. You can tell I’m writing this around lunch time 🙂
Anne

I’m also LCHF, but had struggled a bit in recent months despite “staying on course.”

One thing all of you have left out – is the importance of gut flora.

If your gut health is off-balance, you can still run into many problems with proper digestion, inflammation and other issues – including metabolism and insulin levels.

Recently tried “leveling” the gut flora with pro-biotics and pre-biotics – and WOW I have to say, it has made a huge difference.

“Leaky gut” and other digestive issues due to out-of-whack gut flora is something to consider.

Read the book: The Microbiome Diet by Dr. Raphael Kellman. In a nutshell – it may not matter what diet you’re on or what you put in your mouth, if you don’t have a proper balance of “good bacteria” in your system.

I’ll report back in a few weeks – but getting that straightened out has been life-changing.

That is the problem with diet. So many factors are involved like GI flora, vitamins etc. To concentrate on one factor, which seems to be what happens in nutritional research, leads to the differences in results. Unfortunately this is further confounded by “conflicted” research. Grain is after all very big business.

hobokin, I agree with you. I have read that we have destroyed our gut flora with many toxins. Even if you don’t register as pre-diabetic or diabetic through testing, it does not mean you are not having some insulin resistance or other metabolic issues going on. It can take a while to recover your “gut flora”. If this theory is correct, then the idea that we can balance the good bacteria with the bad, may very well also help us fight those diseases that are killing us or causing long term neurological damage. It is complicated but I see that people actually want more preventative natural answers to our healthcare
.

Mary, you are so correct.
Although going low carb very successfully for the last couple of years, I am of the opinion that it is the removal of toxins from my food that has helped me in regaining such good health. Pure food, in as much as I can source easily, along with mindful and informed thinking of what our body works best on, has got me to this great state of health. Indeed, I have avoided vision tests for 3 years until I was sure this new way of eating (for me, that is) had not interfered with my vision. The outcome? At 67, having overturned all manner of nasties over the last 15 years, my retinal screening showed excellent health, with no disease process, including anything caused by diabetes. My new-found opthalmic optician( oh, what a delight to get a ‘proper’ optician,) has found no abnormalities whatsoever, and no age-related deterioration. I have new specs to correct my vision to 20:20, which is a nice achievement I think, when we hear so many stories of everything “going south” for type 2s.
The natural way of eating must surely be the answer, and I believe it has been responsible for reversing what I was told was the inevitable course of type 2 diabetes……such defeatest poppycock!,,,

My husband and I have been on a LCHF diet since 2009. Actually I only eat meat, fish, and eggs. He eats about 50g of carbs a day. We feel wonderful and our weight is perfect. But we have both developed high cholesterol. His is 389. (HDL 62, LDL 308, Tr 96) Mine is 320. (HDL 66, LDL 242, Tr 62) Before our diet change my cholesterol was 160. We do NOT want to change our diet. Our doctor wants us on statins. Why is our cholesterol so high? Is this something we should be concerned with?

I have read a lot on the subject. From what I can find 275 is about the upper limit for any of the research that says higher is better. I can’t find anywhere where anyone says a number near 400 is fine.

I cannot advise as I do not believe that lipoproteins, whatever they may contain, have any significant causal role in heart disease. I don’t know what my level of any fraction, sub-fraction, sub-sub-sub fraction may be, and I don’t care.

I tend to agree with Dr. Kendrick. It seems to me that the latest test that’s become the darling of cardiologists is that way to keep the cholesterol theory alive.

On the other hand, I do think some of these are markers for something else. For instance, I think a “low” HDL might be a marker for insulin resistance. That’s why i think there is a correlation (in some studies anyway) between “low” HDL and heart disease, but it’s not the low HDL that’s causing the heart disease. It’s whatever it’s a marker for, which I think is high insulin resistance.

The difficulty comes in when you go to see your general practitioner, who immediately wants to put you on a statin because of some “cholesterol” test (while ignoring high fasting blood sugar level for instance). What do you do? Personally, I got a different general practitioner, but I’m not sure the next one isn’t going to do the same thing. They’ve all been brainwashed.

For instance, I went to see my cardiologist (I have idiopathic dilated cardiomyopathy), and he saw I lost a lot of weight and asked me if I’d been exercising. Personally, I don’t believe exercise causes weight loss (I’m with GaryTaubes on this), but everyone else is conditioned to believe it does. I lost weight using a combination of high fat, low carb diet, and intermittent fasting. Both helped my insulin resistance, but particularly intermittent fasting has really helped. See Dr. Jason Fung’s website if you want the theory way. I do exercise, three days per week, but I’ve always exercised and it has not helped me while I gained weight. By the way, I told my cardiologist about the intermittent fasting, but not about low carb, high fat: I didn’t want a lecture on the evils of saturated fat.

Also, if you’re still concerned, you can get a test that measures whether your “cholesterol” (lipoproteins) are “light and fluffy” or “dense” (“light and fluffy” = “good”). See the “Cardio IQ Panel (NMR / VAP)” test here:

These can also give you your LDL-P (LDL particle number, yet another darling test). This is in the US, but I assume you can get a similar test where you are.

Personally, I find all of this very confusing. I just read a study yesterday where Tr/HDL was the best predictor of heart disease, but total cholesterol and LDL were not. It seems as if everyday there is another study saying some factor (lp(a), LDL-P, etc.) is important and other factors are not. LDL-P seems to be the current darling of the cardiologists, but I’ve also read studies indicating it’s not as predictive as thought.

That LDL-P number is “high”. To be honest, I’m not sure anyone knows what’s best to do. If you are concerned and want to bring them down, this post has a discussion about a person with similar numbers and what they did to bring them down:

See the part following this: “In one particularly interesting case, a patient in self-prescribed nutritional ketosis presented to me with an LDL-P of more than 3500 nmol/L (i.e., more particles than could be measured by the NMR machine so the report simply said “>3,500 nmol/L”) despite feeling, performing, and looking great.”

You might try what they did there. I have no idea whether it will work (or if it does work, whether it’ll be beneficial and not detrimental).

Well I dunno. The LCHF works for me. I lost around 35lbs easily and without hunger. I never crave baked goods or sweets. I feel very well despite having been diagnosed with Idiopathic Pulmonary Fibrosis four years ago….have already lived two years beyond my doctor’s estimate and feel the same now as I did then. It may be just good luck, but I also credit my diet for my continued health. My opinion is, if a diet makes you feel better, gives you more energy, makes you look vibrant and just plain healthy, then something is very right about it.
Recently my husband and I ate at a friends who made chili with beans, and baked delicious crusty bread. I couldn’t say no, she’d gone to such a lot of trouble. But it played havoc with my intestines, stomach pains and diarrhea for several days. I am thinking that the bread and beans upset my gut biome as we hadn’t eaten bread and beans for nearly two years. Anyway, I won’t be tempted again.
I don’t know what the guy has his knickers in a twist about, who wrote “The Low Carb Myth’. I took a brief look at the book and didn’t like the confrontational and hostile tone and won’t be paying him the compliment of reading it, or paying for it. What is his agenda anyway, does he have a horse in this race or is he just being contrary for the sake of it? Anyone who doesn’t state his sources is suspect in my opinion.

That is the problem now, isn’t it – medical science and advice is about agendas (and money) not about keeping people well.

Your story reminds me of a few others here who have taken up LCHF – they find that various other ailments have also improved. It makes me wonder just how much damage has been done by pushing people into high carb diets.

FYI: insulin converts about 50% of the carbs we eat into immediate energy, up to 10% go to re-fill glycogen stores, if needed, and 40-50% of carbs are turned to fat and stored. And, insulin reduces our ability to burn stored fat for energy.

I am now well and truly totally confused! After a cardiac arrest on New Year’s eve of all days, I embarked on a new lifestyle, no sat fats, no sugar,no salt and lots of exercise(still ongoing). Lost two stone already(wasn’t obese I hasten to add, just fat(ish). On all the usual package of meds, except statins (which seem to cause awful liver problems, so refused anymore). Just when I’m feeling so smug and fit, it seems I am doing it all wrong! I am frustrated, confused and angry with the medical profession! When I had cancer; for ten months I endured numerous rounds of chemo, radiotherapy and surgery and the resultant horrible side effects(of which there were many). However, it did pass. It was the right thing to do, and the result was I got to live another 12 good years and counting! Why is life so complex and confusing when it comes to the treatment of heart attack/disease? Where’s the honesty in all of this?

Joyce. I know how you feel. If you read this blog you will see that it is the big phamaceutical companies that are dishonest. GPs – I think they are simply brainwashed or too lazy/bust to look things up. Read Dr Kendrick’s book ‘The Great Colestrerol Con’ and his other book “Doctoring Data’ they will help clear up some confusion. Won’t stop you feeling angry with the medical profession though (Dr K excluded).

Joyce, if it works you’re not wrong. I exercise and avoid sugar too, but I no longer fear fat or salt. Low carb seems to work for many or even most people, but it’s not a matter of right or wrong. Maybe you’re different or maybe one or two tweaks in the low carb direction would help even more.

I’m afraid we’ve got ourselves into a real dietary pickle with the utterly failed low fat dogma, but people who’ve taught it for thirty years aren’t going to repent and see the error of their ways. Sadly, it will take time. We went low fat in 1983 and obesity has risen ten fold and diabetes nine fold. In no other field could you get such astonishing bad results and continue with the same policy.

The one piece of advice that remains constant is exercise, so it is good that you can and do do follow that advice!

The fact that you have already discovered that the ‘wonderful’ statin drugs have some horrible side effects – supposedly safe enough to give out to almost everyone beyond a certain age – should tell you a lot about one side in this debate.

I am not a medical doctor, and I only joined this blog because I had severe statin side effects, and was lucky to realise in time.

I suggest you start by reading Dr Kendrick’s two books, because they will give a sense of where all this advice has come from. He simply can’t advise you over the internet, as I am sure you realise, but I think his books tell a powerful message, and they are properly referenced, so he isn’t just stating his opinions.

I am also angry with the higher levels of the medical profession (not the GP’s) and medical research.

“The Academy also expresses concern over blanket sodium restriction recommendations in light of recent evidence of potential harm to the overall population. “There is a distinct and growing lack of scientific consensus on making a single sodium consumption recommendation for all Americans, owing to a growing body of research suggesting that the low sodium intake levels recommended by the DGAC are actually associated with increased mortality for healthy individuals,” !

There are a string of research papers that show that reducing salt intake in the healthy has a minimal effect on SBP – a few mm.Hg. To impose a reduction on the population at large to benefit the few with salt intolerance (kidney damage etc.) is ludicrous. There is also evidence that those on higher salt (<15 mmol.Na) live longer.

I got the book on Kindle. Not worth it. reading Chapter 1 resulted in finding sundry contradictions as well as the “odd result” of the daily increase of 350 calories PER DAY, leading to an increase of intake of 3,800+Kcals by 2000, on top of the intake in 1970. Puzzling.

Some studies seem to show that it’s not just carbs that are the problem, but that sugar with saturated fat is a particularly potent combination for obesity and all the other bad things that come along with that. In other words, saturated fats aren’t exonerated completely, as they seem to exacerbate the effect of consuming excess sugar. I think this interaction might also explain why the low-fat vegetarian/vegan community can get away with eating so many carbs without ill effect. I am wondering if your analysis might be able to shed some light on why that should be the case…

Pauline, good point. We do seem to find the combination of saturated fat and sugar in, say, donuts and biscuits particularly appealing, although we can undoubtedly learn to wean ourselves away from such junk. For example, the taste of sugar in coffee in now repellent to me. However, I think the saturated fat in meat is likely to be very different from the saturated fat found in junk. I don’t know if I really go along with sugar being ‘addictive’, but we do like it and can eat a lot as it doesn’t satiate our appetites.

the combination of saturated fat and sugar in, say, donuts and biscuits particularly appealing,
I suspect that the donuts are cooked in poly-unsaturated oils (and trans-fats) while biscuits (manufactured) often include hydrogenated oils (+trans-fats)

search “Andy Lopez” above. (no 3)

The FDA has finally decided to ban trans-fats from food after 60 years from the time Dr Kummerow first raised the issue.

I find myself doubtful about all dietary studies – I mean, if the medical profession could nuance endless studies to come out with totally wrong guidance for 30+ years, you have to ask if any of these studies are fit for purpose.

Pauline, the way I understand it (And maybe someone can put me straight if I’m wrong) the combination of high carb (sugar in all it’s forms) and high fat, even sat. fat, is absolutely not a good idea. The body must burn up the glucose first as glucose is very toxic, and so just shovels the fat into storage, so you gain weight …at least most people do..and eventually develop metabolic syndrome. I don’t know what the studies are that you refer to, but it seems very odd that they studied high levels of sugar and sat fat together and came out with a conclusion that sat. fat has some negative effects, when most likely it was the high sugars,(sucrose and carbs together). It sounds to me as though the people doing the study were looking for “proof” that sat. fat is bad for us, how on earth could they conclude how much damage either one was doing when they are eaten together? Saturated fat is not the evil doer here, it’s the sugar, and having a high amount of both together is just a recipe for disaster, a very bad combination. I’m curious as to why you think the vegan community can get away with eating low fat and high carb with no ill effects.

Could you list those studies? I hear this “saturated fat is bad in the presence of too much sugar”, but I don’t know what study suggests this. For instance, here’s a huge, long, randomized controlled trial of primarily post-menoposal women:

8 years, one group lowered their fat and saturated fat content, ate more fruits and vegetables, ate less, etc. The study cost somewhere around 420-470 million US dollars. The result? Nothing. There are no statistically significant differences in anything, not heart disease, not cancer, nothing.

Also, there are many studies indicating vegetarians do not fare well. For instance, Dr. Kendrick’s first book relates a bunch of them, as they pertain to heart disease. (I only know this because I’m re-reading his book for the fifth time and happened to read these sections.)

It is actually very hard to eat enough fat on a LCHF diet. One does not notice this at first when one is concentrating on restricting the carbs, but I found after 18 months and around 3 stones weight loss, that my weight loss stalled and I had to examine my fat and protein intake in more detail.
The problem was that high fat foods tend to be high protein foods as well and while my fat intake was usually too low, my protein intake tended to be much too high.
Also, the general opinion seems to be that metabolic rate tends to fall disproportionately fast compared to body weight when dieting. The trick seems to be to keep ones Calorie intake above one’s estimated basal metabolic requirement but below the estimated total required for one’s life-style, very sedentary in my case. These estimates can be calculated, allowing for one’s sex, height and weight, using various methods found on the internet. Keeping a relatively high Calorie intake should stop one’s metabolic rate from plummeting; it should simply fall in line with one’s weight.
I have now managed to lose almost another stone but it is a struggle. We shall see.
What I do not want to happen is to get into the vicious circle where I was GAINING weight on 400 Calories a day, as happened to me 30 years ago. I stopped that diet in despair and put the weight back on within a couple of years. At least, one does not feel hungry on the LCHF diet so I should be able to stick it, even if my weight loss is tailing off.

Dr. Kendrick, this was an excellent blog on the carbs and where they go. I see so much progress being made. The grocery shelves and even frozen foods sections are replete with foods that claim to be low sugar. I guess people are figuring it out, but this post was particularly interesting as you break it down easily for us laypersons as well.

I am wondering if your newest book in out in paperback yet. Want to give them away as gifts as I have my hard cover copy of Doctoring Data. Thanks again!

Hello Marian, I wonder what a paediatric dietician makes of the Tim Noakes complaint and hearing in South Africa. My niece has a two year old boy and asked me if my low carb diet is suitable for him. It’s undoubtedly done me good but I hesitate to advise on children. Good to have your contribution on here.

All I can say here today is that I have learned so much. The books and works of Doctors Graveline and Kendrick were my first intro to the statin dilemma I faced two years ago. I think they were the innovators when it comes to the statin damage crisis. I sure am happy to be alive and am so happy to have all those here whose stories both personal and scholarly, have helped me to figure out what is important. Thanks all. I owe ya one!!!

I think it’s amazing that when the body consumes something that unfriendly bacteria would like to get its hands on, the body produces particles that have an immune function. The design is so elegant and I have to marvel at such things. It’s almost as if we’ve evolved contingent strategies for dealing with a wide variety of foods… or something.

One of the most infuriating arguments I hear from purveyors of extreme diets is ‘just because we evolved on a diet doesn’t mean we can automatically infer it’s the best diet for us’ It’s very hard to argue with and it’s logically ‘true’, but the space it leaves they often try to fill with something so utterly bananas I give up caring. “Fine, eat nothing but lettuce and pineapples then, whatever. Maybe you’ll grow a tail like a lemur.” At least I’d find that entertaining.

But I think I’ll never get used to the unconscious collusion of vegans with the statinators, that one get’s right up my nostril. It’s particularly weird to me as they’re frequently the types most anti industry on many levels, but play pharma and terrifying agribusiness cards with a naivety strong as concrete.

I have a question about bile. Bile acids are mainly derived from cholesterol, and contain some minerals. They are used to help the small intestine absorb fats and whatever is associated to fats, such as vitamins and many fat-soluble substances that the body can use.

Now, many vegans are terrorised by fats. These poor people seem to believe that if they eat any fat they will die a painful and sudden death. They also believe that minerals and salts, such as sodium, are intrinsically evil. I once heard a vegan say that celery is not good for you because it has far too much sodium. Which, of course, is rubbish.

The body can create cholesterol from carbohydrates. So a high-carb, very low fat diet would probably generate enough cholesterol to sustain life. But, perhaps it also generates far too much bile. And, if they don’t eat fats (vegetable or animal), then bile is idle. But when a vegan develops gallstones and that dreaded and painful gallbladder disease (with or without gallstones), they experience an extreme form of cognitive dissonance: “Hey!, I don’t eat fat, I avoid fats like the plague! I shouldn’t be experiencing this pain!”

Is it possible that, in some people, gallbladder disease is related to not eating enough fat, rather than because they ate some fat thirty years ago, when they where young and unenlightened?

Other than eating some butter o coconut oil, is there any treatment to an excess of bile that won’t hurt my friends feelings?

———

For one year I’ve been studying the cholesterol conundrum. I conclude that if one wants to avoid having any cholesterol in the body, then one must follow the half-a-leaf diet, which consists on eating only half a leaf of chard once a month, and no other food. Why half? Because a whole one will be atherogenic, you moron! Also, don’t drink anything, and find some surgeon who will remove the brain from your skull along with the whole nervous system. I guarantee that, with this diet, anyone can (perhaps) live a cholesterol-free life. Once you achieve that, you can start living and being happy.

In the week that I attended the funeral of a 60 year old, who recently developed diabetes and died of infections spreading from a urinary tract infection (oh and was on cholesterol lowering drugs, surprise, surprise), I heard glowing tributes to Professor Michael Oliver on Last Word. He allegedly proved the link between cholesterol and heart disease, which led to the development of life saving statins.

I think there is a real danger that all the insights into saturated fat, cholesterol, and statins, gained in recent years, might get buried again – not because they are wrong, but because they are inconvenient.

We seem to have developed a new kind of propaganda – one based on excessive respect by the media for scientists.

Don’t air alternative medical opinions – or even allow them to be debated – in case people harm themselves by accepting anything other than the orthodox position.

Don’t let alternative ideas about the climate surface, just in case people begin to loose their belief in Climate Science, and destroy the planet!

Think of “Doctoring Data” – surely that book should be worth a serious debate on TV/radio. Why would journalists shy away from a subject like that? Unfortunately, it is much easier to spread propaganda in a country that believes it has a free press!

If the BBC was doing its job as it used to do, I think both these orthodoxies would be on their knees by now.

I’ve just been asked my opinion on this blog, and have already posted a couple of comments above. I’d like to task you with looking at a couple of other areas – especially what you term:

“This is basic, incontrovertible science.”

DNL does not seem to happen to any real extent in the human body. DNL to any extent doesn’t occur in humans, and has been known to biochemistry for some time. Reference books showing that DNL is not a pathway invoked in humans to any real extent include Metabolic Regulation by Frayn, and Biochemistry for Sports and Exercise Science by McLaren and Morton.

The insulin hypothesis also has been thoroughly debunked – insulin is nothing more than an adaptive response. Many amino acids and ingested proteins have a high insulin response, beef being similar to white rice for example. Fat ingestion also helps ‘prime’ insulin for release. So carbohydrates aren’t in themselves uniquely fattening, and even in the absence of carbs ASP will stimulate the insulin required for storage.

Insulin may be the storage hormone as one of its functions – however, it is not the reason ‘why we get fat’. Chronic overnutrition is. If we overeat any macronutrient, or all lol, then we’ll get fat.

Further, whilst it is true that there isn’t epidemiological evidence of correlation between saturated fat and cardiovascular heart disease, intervention studies since the 30’s have show a straight line increase in risk with saturated fat dietary increase. Saturated fat hasn’t got the all clear either.

Dr Dr Kendrick,
I have this blog four times, I found it so clear and well explained.
i have a question. As I understand it, surplus carbs, all convert to sugar, and then, if still surplus, converted into palmitic acid and stocked. Palmitic acid is a SFA and a major component of breast milk. Why is it that palm oil arouses such passion as being bad for you, since it contains, the same palmitic acid as well as oleic acid, a large constituent of Olive oil. I leave aside the environmental aspects, undoubtedly bad, but the product itself. My lipids doctor goes pale when I mention it, and almost gets me to rinse my mouth out with and antiseptic for using very bad language?

I’ve been thinking a lot about the mechanisms you’re describing here and the dogma surrounding this stuff. It’s insane that governments and “experts” around the world simultaneously came up with the ideas that people need to consume a whole bunch of carbohydrates AND keep their LDL levels low. When you think about it, the only way a person can hold these two competing beliefs is if they are dogmatic.

If excess carbs leads to adipose buildup, how do people on HCLF diets (90% carbs – 5% fat – 5% protein) manage to stay thin?
Here’s an example of a lady who does a very HC diet: http://rawfoodsos.com/
You may enjoy the blog post as well.

Yes, but aren’t hormones more critical than simple calorie counting when it comes to weight loss? If the answer is yes, then (in my opinion, and it changes once in awhile) a person is using a terrible method to lose fat tissue and is most likely doing it at the expense of their general health because hormones are one of the most critical components in our physiology, and when they’re out of wack, it sets the stage for chronic degenerative diseases.

I honestly do not believe that a person could exercise enough to burn a meaningful amount of calories to stay thin, at least during the exercise itself. Hormones are trump for weight loss, and if someone is staying thin that means there are mechanisms not being accounted for. Thermogenic, digestive, UTM, there’s many factors that affect the RMR. I apologize, I thought I’d get a different answer from you.

That’s Denise Minger’s website. She’s a former vegan who stopped eating that way because of negative health effects. I don’t think most people would call her HCLF – she did a writeup recently about some benefits of a very low fat diet – in particular, increased insulin sensitivity. One of the things she’s best known for is her writeup of “Forks over Knives”, and problems in the China Study.

Well she just did a podcast with Ben Greenfield about a month ago explaining her diet, and if you seriously don’t call 90% calories from carbs “high-carb” we don’t have a lot to talk about. And yeah, I read her article. Honestly? It seems like there’s potential there. But I guess we’ll see.

Someone mentioned Unger/Glucagon in the comments of an earlier thread, just found fulltext by Unger H R and Cherrington A D

“Glucagonocentric restructuring of diabetes: a pathophysiologic and therapeutic makeover”

Don’t know whether it’s the same paper or later upgrade, may be useful perhaps, found via Peter D. @ high-fat-nutrition

Re Carbs turning into fairies.. there is a way, the polyol pathway, it leads to evil fairies damaging cells osmotically (retina etc)
Of course that won’t help with the LDL. My impression is that fats and carbs simply cannot be burnt well at the same time. They downregulate each other. Via insulin, and palmitic acid to counteract. So the fatophobes have sort of a point. It even seems you can escape some of the damage by eating more carbs and get into ‘carbosis’. Again, Peter is just invaluable for these things.

I read once that alcoholics have very clean arteries. Unfortunately this was a reader’s letter in a joke magazine. It would maybe take clinical experience which I only have at the receiving end of quackery to figure out whether there could be anything to it. Maybe poor man’s hypoglycaemia drug?

Dr. Kendrick, I am struck by the lack of attention to the evolved role of apo C-III in carbohydrate intolerance (i.e. metabolic syndrome). The liver produces apoB100 Tg carriers (VLDL) with apoC3, and the small intestine produces apoB48 Tg carriers WITHOUT apoC3.
ApoC3’s role is to slow and inhibit the entire process of delivering hepatic de novo Tg’s to adipocytes, presumably because we are evolved to see very little of this but a lot of dietary Tg’s. Since the postprandial nutrient absorption process is time-critical and involves a mix of macronutrients, delivery of dietary Tg’s is HEAVILY favored in the NORMAL modern hominid (i.e. us). We are supposed to be able to easily store the carb-derived excess in our dietary OFF time (i.e. while fasting).
It is no wonder that we can reach a level of saturation in delivering carb-derived Tg’s to fat tissue with modern diet — the amount of carb is well outside of evolutionary context.
The “paradox” comment you referenced (Parks) presumes a level playing field for the de novo Tg’s vs. the dietary Tg’s. But it is NOT so, by DESIGN (i.e. evolution). THAT is why storing more fat from carb’s than from dietary Tg’s is pathological even in the most carb-tolerant, no?

What you are saying is partly true. If you eat a high fat diet containing saturated fats, the chylomicrons will eventually be converted to chylomicron remnants, after delivering fats to tissues, and go to the liver. These remnants are mostly TGs that can potentially increase VLDL production as well, which turns to LDL as you explained. So a high fat diet may also be detrimental leading to increased risk of CVD. What do you think?

I greatly liked the way you explained things but I wanted to point out this piece of information that You did not mentioned. Thanks greatly!

I went back (with a vengeance) to low/zero carbohydrate, high fat, moderate protein on March 16, 2016. My weight was 93.4 kg (206 lb). My waist was 106.7 cm (42 in). Height was 180.3 cm (71 in), and is still the same today. BMI was ~30.
Today I weigh 57.15 kg (126 lb). Waist today is 83.82 cm (33 in). BMI is ~20.
I will never, ever, ever, ever, ever turn back to the poisons that were killing me early in my 65th year.
I’ve been asked if I had cancer, if I was “sick”, if I was “dying”.
A few have ventured to ask, “How are you doing it?” I always reply directly and straightforwardly, “I stopped eating the poisons.” Then I will do nearly anything to explain that the poisons are carbohydrates (starches and sugars) of more than 50 g/day and polyunsaturated vegetable oils. I have been told matter-of-factly, “Well, you certainly can’t eat fried foods,” to which I reply, “Oh, but I certainly do, and a lot of them.” If they don’t ask, I tell them, “I fry in lard, butter, tallow, avocado oil, coconut oil, walnut oil, rarely sesame or olive oil, any oil that’s saturated or monounsaturated.”
No apologies, to anyone, now or ever about this! No apologies to the “friends” and “wife” I’ve lost since last March: No great loss.
This is my lifestyle for eating.
(And many, many thanks for multiple posters at Karl Denninger’s market-ticker.org forum! They are all such encouragers, the kind of people with whom I want to have conversations. Kudos to Karl and the gang.

Another striking topic lacking much attention by most, but not all, researchers is adipose DNL (de novo lipogenesis). It is pretty clear that the ability to handle large amounts of carb’s, inasmuch as any of us have it in youth or otherwise, is completely dependent upon this pathway. Glycogen storage capability in humans is trivial at any age — he who thinks otherwise has to do a few simple calculations. And hepatic DNL only is upregulated once adipose tissue storage has been saturated, and is pathological (i.e. metabolic syndrome):http://www.asbmb.org/asbmbtoday/asbmbtoday_article.aspx?id=15872
Also, see research by Iizuka et al.
For most of us, by some time in middle age adipose storage will be saturated without adequate carb restriction, leading to metabolic syndrome, etc. Modern hominids (homo sapien and home erectus) were pure meat eaters — this is our current evolutionary state as an animal species. Only those with adequate recent ancestry and exposure to agriculture have been able to adapt epigenetically (via imprint, etc.) to handle modern refined-food quantities for a lifetime.

Dr Kendrick cannot provide individual patient advice over the Internet. UK General Medical Council regulations are clear that to do so would be a breach of medical standards that could result in disciplinary proceedings.

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